15 Gallbladder, pancreas, liver & spleen - primary surgery · 15 Gallbladder, pancreas, liver &...

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285 285 15 Gallbladder, pancreas, liver & spleen 15.1 Introduction The gallbladder may be diseased due to stones, ascaris (15.6), infection per se, tumour or volvulus. The frequency of these diseases varies from region to region, but stones are more common in women than in men, and especially in obese, parous women >40yrs (fat, fertile, female over forty). Gallstones are found in c.80% of adults with sickle cell disease. Many patients are found at postmortem to have gallstones which have caused no symptoms. Just because someone has gallstones, they may not be the cause of dyspepsia! Stones or thick biliary sludge may however pass into the common bile duct and cause biliary colic, or obstructive (cholestatic) jaundice. Stones can promote infection of the gallbladder and cause acute or chronic cholecystitis, although this can arise de novo especially with HIV disease. Stones, especially in the form of gravel (sludge), can also promote infection in the biliary tree, especially in association with obstruction (cholangitis, 15.7) though this may also arise de novo; they can also obstruct drainage of the pancreas and cause pancreatitis. Rarely stones may fistulate into the small bowel and cause obstruction therein. You can usually treat acute cholecystitis non-operatively (15.3), but if this fails, you can drain the gallbladder by doing a cholecystostomy. If you are experienced enough, you can treat chronic cholecystitis by removing the gallbladder (15.8). If obstructive jaundice is due to carcinoma of the head of the pancreas, you may be able to relieve the symptoms by bypassing the obstruction and performing a cholecysto-jejunostomy (15-5), but the situation is more complicated if the obstruction is due to gallstones, ascaris, clonorchis sinensis (Chinese liver fluke) or tumour obstructing the bile duct. You can usually treat acute pancreatitis non-operatively (15.13), but a pancreatic abscess (15.15), and a large pancreatic pseudocyst (15.14) need drainage. You will not be able to remove a pancreatic carcinoma, which may be very difficult to differentiate from chronic pancreatitis. Likewise you will not be able to remove tumours of the liver whether primary (hepatoma) or secondary except with sophisticated equipment, and only when presenting early. However you will be able to treat hepatic tuberculosis. You may have to drain liver cysts, and may need to remove large hydatid cysts carefully (15.12). You may need to drain liver abscesses especially if they are large (15.10), and likewise splenic abscesses (15.18), which you can usually best deal with by splenectomy. This is also indicated for a number of diseases, other than for trauma (15.17). Splenic tuberculosis is usually only diagnosed after you have removed the spleen! 15.2 Biliary colic Biliary colic is due to a stone or sludge impacting in the cystic duct. Very rarely it may be due to volvulus of the gallbladder. There is severe colicky epigastric pain which radiates to the right subcostal region and right scapula. The patient wants to bend herself double, she rolls around, and rarely keeps still. Intense pain comes in waves against a background of a dull ache, typically in attacks lasting about ½hr, 1-3hrs after a fatty meal. Pain makes breathing difficult and may be accompanied by nausea and vomiting. Attacks occasionally last as long as 6hrs. If unrelieved >24hrs, cholecystitis develops. There may be tenderness in the hypochondrium or the right epigastrium, and be a +ve Murphy's sign (15.3). ULTRASOUND is a simple, cheap and accurate way of finding stones in the gallbladder, whether or not there is jaundice: they cast an ‘acoustic shadowbehind them (38-5). Occasionally you might find ascaris in a bile duct (15.6). N.B. RADIOGRAPHS. Most gallstones do not show up, so a plain film is unlikely to help. DIFFERENTIAL DIAGNOSIS OF BILIARY COLIC Suggesting ureteric colic: pain radiating towards the groin and genitalia. Blood in the urine on microscopy. Radio-opaque calcifications on abdominal radiographs along the line of the ureter. Suggesting right basal pneumonia: cough, fever, and lung signs at the right base. Suggesting upper small bowel obstruction: central colicky pain with profuse unrelieved vomiting. NON-OPERATIVE TREATMENT OF BILIARY COLIC. Treat with pethidine 50-100mg 3-hrly IV or IM, for 24-48hrs. Hyoscine 20mg may help. Restrict to clear fluids only by mouth. If vomiting ensues, replace fluids IV. Normally, pain will stop in 24-48hrs, and you can start feeding cautiously, avoiding oily or fatty foods. If symptoms persist >24hrs with tenderness in the right hypochondrium, acute cholecystitis has developed. 15.3 Acute cholecystitis Symptoms are often initially those of biliary colic (15.2), but they last >24hrs and pain becomes constant. There is a very good chance of recovery in 10days, even without treatment. There is a 5% chance that (1) the infection will build up in the gallbladder to produce an empyema, (2) peritonitis will develop, (3) a fistula into bowel will occur from a perforation of the gallbladder. Recurrent episodes of cholecystitis are likely in >50%.

Transcript of 15 Gallbladder, pancreas, liver & spleen - primary surgery · 15 Gallbladder, pancreas, liver &...

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15 Gallbladder,

pancreas, liver &

spleen

15.1 Introduction

The gallbladder may be diseased due to stones, ascaris

(15.6), infection per se, tumour or volvulus. The frequency

of these diseases varies from region to region, but stones

are more common in women than in men, and especially in

obese, parous women >40yrs (fat, fertile, female over

forty). Gallstones are found in c.80% of adults with sickle

cell disease. Many patients are found at postmortem to

have gallstones which have caused no symptoms.

Just because someone has gallstones, they may not be the

cause of dyspepsia! Stones or thick biliary sludge may

however pass into the common bile duct and cause biliary

colic, or obstructive (cholestatic) jaundice. Stones can

promote infection of the gallbladder and cause acute or

chronic cholecystitis, although this can arise de novo

especially with HIV disease. Stones, especially in the form

of gravel (sludge), can also promote infection in the biliary

tree, especially in association with obstruction

(cholangitis, 15.7) though this may also arise de novo;

they can also obstruct drainage of the pancreas and cause

pancreatitis. Rarely stones may fistulate into the small

bowel and cause obstruction therein.

You can usually treat acute cholecystitis non-operatively

(15.3), but if this fails, you can drain the gallbladder by

doing a cholecystostomy. If you are experienced enough,

you can treat chronic cholecystitis by removing the

gallbladder (15.8). If obstructive jaundice is due to

carcinoma of the head of the pancreas, you may be able to

relieve the symptoms by bypassing the obstruction and

performing a cholecysto-jejunostomy (15-5), but the

situation is more complicated if the obstruction is due to

gallstones, ascaris, clonorchis sinensis (Chinese liver

fluke) or tumour obstructing the bile duct.

You can usually treat acute pancreatitis non-operatively

(15.13), but a pancreatic abscess (15.15), and a large

pancreatic pseudocyst (15.14) need drainage.

You will not be able to remove a pancreatic carcinoma,

which may be very difficult to differentiate from chronic

pancreatitis. Likewise you will not be able to remove

tumours of the liver whether primary (hepatoma) or

secondary except with sophisticated equipment, and only

when presenting early. However you will be able to treat

hepatic tuberculosis. You may have to drain liver cysts,

and may need to remove large hydatid cysts carefully

(15.12). You may need to drain liver abscesses especially

if they are large (15.10), and likewise splenic abscesses

(15.18), which you can usually best deal with by

splenectomy. This is also indicated for a number of

diseases, other than for trauma (15.17).

Splenic tuberculosis is usually only diagnosed after you

have removed the spleen!

15.2 Biliary colic

Biliary colic is due to a stone or sludge impacting in the

cystic duct. Very rarely it may be due to volvulus of the

gallbladder. There is severe colicky epigastric pain which

radiates to the right subcostal region and right scapula.

The patient wants to bend herself double, she rolls around,

and rarely keeps still. Intense pain comes in waves against

a background of a dull ache, typically in attacks lasting

about ½hr, 1-3hrs after a fatty meal. Pain makes breathing

difficult and may be accompanied by nausea and vomiting.

Attacks occasionally last as long as 6hrs. If unrelieved

>24hrs, cholecystitis develops. There may be tenderness in

the hypochondrium or the right epigastrium, and be a

+ve Murphy's sign (15.3).

ULTRASOUND is a simple, cheap and accurate way of

finding stones in the gallbladder, whether or not there is

jaundice: they cast an ‘acoustic shadow’ behind them

(38-5). Occasionally you might find ascaris in a bile duct

(15.6).

N.B. RADIOGRAPHS. Most gallstones do not show up,

so a plain film is unlikely to help.

DIFFERENTIAL DIAGNOSIS OF BILIARY COLIC

Suggesting ureteric colic: pain radiating towards the

groin and genitalia. Blood in the urine on microscopy.

Radio-opaque calcifications on abdominal radiographs

along the line of the ureter.

Suggesting right basal pneumonia: cough, fever,

and lung signs at the right base.

Suggesting upper small bowel obstruction: central

colicky pain with profuse unrelieved vomiting.

NON-OPERATIVE TREATMENT OF BILIARY COLIC.

Treat with pethidine 50-100mg 3-hrly IV or IM,

for 24-48hrs. Hyoscine 20mg may help.

Restrict to clear fluids only by mouth. If vomiting ensues,

replace fluids IV.

Normally, pain will stop in 24-48hrs, and you can start

feeding cautiously, avoiding oily or fatty foods.

If symptoms persist >24hrs with tenderness in the right

hypochondrium, acute cholecystitis has developed.

15.3 Acute cholecystitis

Symptoms are often initially those of biliary colic (15.2),

but they last >24hrs and pain becomes constant.

There is a very good chance of recovery in 10days, even

without treatment. There is a 5% chance that

(1) the infection will build up in the gallbladder to produce

an empyema,

(2) peritonitis will develop,

(3) a fistula into bowel will occur from a perforation of the

gallbladder. Recurrent episodes of cholecystitis are likely

in >50%.

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In HIV disease, the gallbladder can be markedly inflamed

without the presence of stones (acalculous cholecystitis).

This is due to cryptosporidia or cytomegalovirus in 20%,

and produces an ischaemia of the gallbladder wall.

Infection may also be present with salmonella; in typhoid,

organisms infect the gallbladder but cholecystitis is often

masked by generalised peritonitis. Cholecystitis without

stones may also be caused by brucellosis, dengue,

leptospirosis & campylobacter.

Stones may be in the gallbladder but also in the bile duct

and cause partial or complete obstruction with jaundice or

cholangitis. Biliary débris at the sphincter of Oddi may

result in pancreatitis.

Operate if:

(1) there is cholangitis which is life-threatening,

(2);the gallbladder forms a gradually enlarging acute

inflammatory mass,

(3);there are repeated attacks leading to chronic

cholecystitis.

The acutely inflamed gallbladder is oedematous,

and perhaps gangrenous, and often adherent to

surrounding structures, so do not try to remove it unless

you are experienced. Instead, drain it (cholecystostomy).

This may be life-saving and is simple and safe, but it may

not cure the disease permanently, so you may have to think

of a cholecystectomy later.

N.B. Never try to repair a perforation in an inflamed

gallbladder.

Repeated attacks of acute inflammation are usually less

severe than a typical acute attack. Symptoms may subside

without infection and leave the gallbladder shrunken and

fibrosed. However, if a stone remains impacted in

Hartmann’s pouch (15.4, 15-3M), the gallbladder will

distend with fluid (mucocoele of the gallbladder) and if

this becomes infected, the subsequent distension with pus

(empyema of the gallbladder) may cause it to burst.

SIGNS.

The patient is febrile, looks sick, and lies still. There is

well localized tenderness in the right upper quadrant.

There may be exquisite tenderness (unlike biliary colic),

with guarding and rigidity. Murphy's sign is usually +ve:

MURPHY'S SIGN. Put your hand under the ribs on the right side, and ask the patient to take

a deep breath. If she feels pain as the gallbladder moves down on to your

hand, the sign is +ve and indicates cholecystitis.

A well-localized mass sometimes forms a few days after

the start of the attack, just below the right costal margin.

Mild jaundice does not always mean that the common bile

duct is obstructed by a stone. If there is jaundice, swinging

fever, chills and rigors, however, suspect cholangitis.

SPECIAL TESTS. There is a leucocytosis, unless there is

untreated HIV disease. The serum bilirubin and alkaline

phosphatase will only be raised if there is obstruction of

the biliary tree. The amylase & lipase are raised in

pancreatitis.

ULTRASOUND. Gallstones readily show up with an

‘acoustic shadow’. With experience you will be able to

see if the common bile duct is dilated and if more stones

are found inside the duct. The presence of stones may

imply cholecystitis, but does not prove it. To confirm the

diagnosis, you need to see a thickened gallbladder wall

and/or fluid around the gallbladder (38.2B).

Fig 15-1 CHOLECYSTOSTOMY.

A, right subcostal (Kocher’s) incision. B, insert a purse string suture.

C, aspirate the gallbladder. D, remove the stones. E, insert a Foley

catheter. Kindly contributed by Gerald Hankins.

DIFFERENTIAL DIAGNOSIS OF ACUTE CHOLECYSTITIS

Suggesting liver abscess (15.10): tender hepatomegaly

with fever and previous diarrhoea and dry cough.

Suggesting perforated peptic ulcer (13.3): sudden onset

of extreme constant pain, with previous dyspepsia.

Suggesting acute pancreatitis (15.13): pain radiating to

the back, with alcohol abuse.

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Suggesting acute pyelonephritis: pain in the flank

associated with urinary frequency, haematuria and

previous ureteric colic or schistosomiasis.

Suggesting volvulus of the small bowel with

strangulation (12.8): initial colicky pain which then

became constant, associated with abdominal distension,

tenderness and guarding.

Suggesting perihepatitis (Curtis-Fitzhugh syndrome):

previous episodes of PID, especially with HIV disease.

Suggesting haemorrhage in a liver tumour: tender knobbly hepatomegaly with weight loss and

anorexia.

NON-OPERATIVE TREATMENT FOR ACUTE

CHOLECYSTITIS Make sure of the diagnosis with ultrasound (38.2B) and

repeated examination. Perform an OGD (13.2) if you can,

to exclude reflux oesophagitis, gastritis or peptic

ulceration as differential diagnoses.

Treat pain with enough opioid: e.g. pethidine (50-100mg

3hrly). Nasogastric suction is not essential, but it will keep

the stomach empty and so relieve nausea and vomiting.

Keep nil orally. Correct the initial fluid loss with IV saline.

Antibiotics are less necessary than you might expect,

because the inflammation in the gallbladder is primarily

chemical. However they probably reduce complications:

treat with chloramphenicol (or gentamicin), ampicillin,

or doxycycline. Continue this treatment till the pain and

pyrexia settle; then introduce oral fluids and after this

allow a fat-free diet. Symptoms should start to improve

after 24hrs, and disappear in 3wks. Advise a low-fat diet,

and review after 2-3 months.

If symptoms recur, repeat the treatment for acute

cholecystitis. When things have settled, think about an

elective cholecystectomy, usually six weeks afterwards,

if stones are definitely present. Do not operate for

acalculous cholecystitis unless there is marked tenderness

and you fear imminent perforation.

15.4 Empyema of the gallbladder

When cholecystitis gets worse, the gallbladder enlarges

and becomes a tense inflammatory mass. This may occur

if the cystic duct is obstructed with a gallstone, or

secondary to carcinoma. The gallbladder fills with pus

and so becomes an empyema; it then may perforate

resulting in septic biliary peritonitis which is frequently

fatal.

The patient is sick, pyrexial, lies still and has a painful

tender mass in the right hypochondrium below the liver.

There may be a known history of gallstones, but usually

not of jaundice.

SPECIAL TESTS. Leucocytosis progresses from earlier in

the disease. Amylase is usually normal.

ULTRASOUND. The gallbladder is filled with turgid

fluid, and often gallstones; its wall is thickened (38.2B).

Aspiration may relieve some symptoms in a very sick

patient, but is not a lasting solution.

CHOLECYSTOSTOMY (GRADE 3.3)

INDICATIONS. Drain the gallbladder if:

(1) intense pain persists with swinging fever,

(2) abdominal tenderness gets worse, the area of guarding

extends, or the mass increases in size both suggesting an

empyema of the gallbladder,

(3) there is cholangitis with a distended gallbladder (15.7),

(4) the patient is too sick to undergo a cholecystectomy.

ANAESTHETIC. If the patient is very sick or very old you

can operate under LA, especially if the gallbladder is tense

and easily palpable under the abdominal wall.

PREPARATION. Make sure your suction is working

properly. Treat with gentamicin and metronidazole.

INCISION. Feel for the area of maximum tenderness,

an ill-defined mass, or both (15-1A). Centre the incision

over this area, and cut through all layers of the abdominal

wall 2cm below and parallel to the line of the costal

cartilages. You will probably find the gallbladder easily.

If you do not find it, carefully separate the adherent

omentum and transverse colon by pushing them away with

your finger. Pack away the rest of the abdominal contents

away from the inflamed gallbladder. This will be easier if

you tilt the table feet down. Handle the gallbladder

carefully; it easily ruptures and spills infected bile into the

peritoneal cavity.

If the structures below the right lobe of the liver are matted

together in an oedematous haemorrhagic mass, so that the

gall bladder is difficult to find, insert your hand over the

upper surface of the liver, and draw your fingers down

until you reach its edge. Then move your hand medially

over the convex surface of the liver until you reach the

falciform ligament, joining the liver to the diaphragm.

At its lower edge is the ligamentum teres. About 5cm to

the right of this, you should be able to feel the tense,

turgid, elongated mass of the fiery-red, acutely inflamed,

oedematous, and perhaps partly necrotic gallbladder.

Try to expose enough of the fundus of the gallbladder to

allow you to drain it. Use your finger, or a 'swab on a stick'

(4-9A), to 'peel' the omentum, the hepatic flexure of the

colon, and the transverse mesocolon carefully out of the

way. Avoid sharp dissection. If there is bleeding, control

the haemorrhage with packs.

Put a purse-string suture on the gallbladder fundus

(15-1B), incise it and aspirate the pus (15-1C).

Then enlarge the opening and extract as many stones as

you can (15-1D); if they are very adherent in Hartmann’s

pouch (15-3M), leave them, rather than perforating the

gallbladder. Do not attempt to explore the common bile

duct.

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Place a wide-bore catheter, which you have inserted

through a separate stab incision in the lateral abdominal

wall, in the gallbladder, and close the opening around the

catheter snugly with 2 purse-string sutures, one 5mm away

from the other (15-1E). Secure the catheter drain and

attach it to a drainage bag. Lavage the abdomen with warm

water.

DIFFICULTIES WITH EMPYEMA OF THE GALLBLADDER

If you cannot reach the inflamed gallbladder,

extend your incision across the midline as an inverted-V.

If you do not find a tense inflamed gallbladder at operation, look for differential diagnoses and act

appropriately.

If the gallbladder is not that seriously inflamed,

and you are able to do so, perform a cholecystectomy

(15.8).

If you rupture the gallbladder at Hartmann’s pouch (15-3M), which is a mucosal fold between the neck of the

gallbladder and the cystic duct, sometimes caused by

adhesions between them, where gallstones commonly get

stuck. It may be present in both normal and pathological

gallbladders. Try to remove any impacted stone (which

should be freed up by your manipulations) and if possible

put a ligature around the cystic duct remnant. Remove as

much of the inflamed gallbladder as you can (if the

posterior wall is very adherent to the liver, leave it)

and insert a wide-bore drain through a separate stab

incision in the abdominal wall.

If the gallbladder is so tense and inflamed and a suture

causes it to leak profusely, apply suction and remove as

much of the inflamed gallbladder as you can, as above.

If the gallbladder has already perforated, there is

already effectively a cholecystostomy and friable tissues

will make cholecystectomy too difficult. Aspirate septic

fluid from the abdomen and pack away the bowels.

Remove as much of the gallbladder wall as possible: you

can leave the posterior wall adherent on the liver surface.

Remove any debris and stones. Try to close the cystic duct

with an absorbable suture if you can. Leave a drain

brought out through a separate stab incision.

Fold some omentum into the bed of the gallbladder.

POSTOPERATIVELY, expect bile to start draining in a

day or two. Chart the daily amount of bile draining.

Plan to remove the tube in 14days. If the bile is still

discharging after 2wks however, leave the catheter in situ

for a month at least before removing it. If the bile loss is

significant, replace fluid and electrolytes IV. You can try

to return the bile to the intestines via a nasogastric tube if

the patient will tolerate it. The fistula will slowly close

unless a stone has been left in Hartmann’s pouch (when a

small mucous fistula will result, 15-3M).

N.B. The cholecystectomy needed to cure this problem

may be difficult indeed.

15.5 Cholangitis

Ascending cholangitis describes infection in the bile duct,

which if untreated, may be followed by multiple abscesses

in the liver, or by septicaemia. IV antibiotics are

necessary, but if stones are the underlying cause,

the common bile duct should be explored, and any stones

removed. This is difficult and needs special instruments

and on-table radiography. If it is impractical, and the stone

is distal, you may still be able to decompress

the common bile duct by inserting a T-tube

(choledochostomy), or by opening the duodenum and

opening the sphincter of Oddi wide, but this is difficult

surgery.

A patient with cholangitis usually has a previous history of

biliary colic and cholecystitis. Typically, an attack of colic

is followed the next day by fluctuating jaundice, dark

urine, pale stools, nausea and vomiting, fever and rigors.

The liver may be tender, but the gallbladder is not

palpable.

In HIV disease, cholangitis may occur intermittently

without the presence of stones, mimicking primary

sclerosing cholangitis. In East Asia, liver fluke infestation

often causes cholangitis (15.7). In endemic areas, consider

hydatid disease.

SPECIAL TESTS. Check if ascaris ova are in the stool:

this does not necessarily mean that worms are the cause of

cholangitis, but strongly suggests it (15.6).

ULTRASOUND (38.2) is very useful to confirm the

presence of stones, cysts or ascaris and their number and

position in a dilated common bile duct.

CHOLEDOCHOSTOMY (GRADE 3.5)

PREPARATION

Treat with IV ampicillin, gentamicin and metronidazole,

or substitute ampicillin & gentamicin with a

cephalosporin, ciprofloxacin, or mezlocillin.

If he is septicaemic, resuscitate the patient with Ringers

Lactate. Add Vitamin K 10mg IM. Insert a nasogastric

tube. Do not delay.

INCISION. Make an upper midline incision and follow the

initial steps to find the gallbladder (15.3), then expose the

subhepatic area, cystic duct, and common bile duct.

(The midline incision is better for exposure of the common

bile duct than a subcostal incision).

Expose the biliary tree as in a cholecystectomy (15.8),

but without grasping the gallbladder. Make sure you have

found the bile ducts before proceeding further.

Palpate them to be sure none of them pulsates! If in doubt,

aspirate the common duct to make sure it contains bile and

not blood. Then expose 2cm of the common bile duct,

which will probably be significantly dilated (>5mm)

(15-2A), and place two 3/0 stay sutures on its anterior

surface about 4mm apart (15-2B). With the tip of the

sucker close by, make a longitudinal incision, between the

stay sutures (15-2C). Suck out all the bile and exudate, and

take a swab for culture and sensitivity.

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Using Desjardin's stone forceps, gently remove any stones

that you can easily see (15-2D). The curve on the forceps

may help you: the stones are probably well down the

common duct at its lower end, where it enters the

duodenum. Do not prolong this stage of the operation if it

is difficult: you can do much harm. If there is much

'sludge', wash out the common duct by irrigating it with

plenty of saline using a plain rubber catheter and a 20mL

syringe.

Fig. 15-2 CHOLEDOCHOSTOMY.

A, expose the common bile duct. B, insert stay sutures. C, incise the

common bile duct. D, remove the stones. E, insert a Fogarty catheter.

F, T-tube sewn in place. G, a T-tube.

EQUIPMENT. FORCEPS, gallstone, Desjardin's. Use these long slender forceps for removing stones from the biliary system.

If you do not have Desjardin's stone forceps, a Fogarty balloon catheter,

pushed past the stone, inflated, and withdrawn is often as effective and less traumatic. You may possibly be able to use a tiny Foley catheter.

Find 2 assistants in addition to the scrub sister.

Insert a T-tube (15-2E), and close the opening in the duct

snugly round the drainage tube with a transverse

absorbable 4/0 suture (15-2F).

Bring the tube out through a stab incision, leaving some

slack inside, in case it is pulled on. Anchor it securely to

the skin with a non-absorbable suture. (You can make your own T-tube by slitting the end of a piece of ordinary suction tubing, and cutting away ⅓ the circumference of the tubing.)

Close the abdominal wall carefully: the wound is likely to

break down or become infected, so consider leaving the

skin open (11.10, 11-20).

POSTOPERATIVELY, connect the T-tube to a bedside

bottle, and allow it to drain freely until the jaundice and

fever subside. Perform a tube cholangiogram 10-14days

postoperatively using 25% sodium diatrizoate (‘hypaque’)

or similar aqueous contrast medium diluted 1:2 with 0·9%

saline. Make sure you do not inject any air with the

contrast medium. If you see no stones, and the medium

flows nicely into the duodenum, clamp the tube.

Provided that there is no pain, fever, or jaundice after 1wk,

remove the tube.

If the cholangiogram shows blockage of flow into the

duodenum or any residual stones as filling defects,

try flushing the duct with 1l of warm saline suspended 1m

above the patient, after treating with hyoscine 20mg IM.

If this fails, check what pressure builds up. It should not be

higher than 8-10cm of water. If after 24hrs no higher

pressure develops, try clamping the tube. Remove it after

2wks if no discomfort develops. If pressure does build up

in the tube, do not remove it. You may then be able to

remove residual stones by dilating the T-tube tract

and pulling them out with endoscopy forceps

(the Burhenne technique), or they can be removed by an

expert by passing a side-viewing fibre-optic endoscope

into the duodenum and slitting the sphincter of Oddi,

or by opening the duodenum at laparotomy.

TRANSDUODENAL ODDI SPHINCTEROTOMY

(GRADE 3.5)

INDICATION. When a stone is impacted at the distal end

of the common bile duct; when antegrade extraction or

lavage has failed to dislodge a stone.

INCISION. Expose the biliary tree as before; then

mobilize the duodenum by the Kocher’s manoeuvre (13.5).

Make a 4cm longitudinal incision in the lateral surface of

the duodenum at the junction of first and second parts, and

feel the papilla with your finger through the duodenotomy.

If you can’t find it, pass a bougie or catheter down through

the common bile duct. Then insert a fistula probe into the

papilla and open it upwards with a #11 blade (4-1) to free

any impacted stones. When you see bile flowing freely

you know you have relieved the obstruction.

Carefully spatulate the edges of the papilla open with

absorbable 4/0 sutures. Be careful not to damage the

pancreatic duct (usually visible at the 5 o’clock position).

Close the duodenotomy transversely in 2 layers with

long-lasting absorbable 2/0 sutures, and cover this with

omentum if possible.

If the bile duct has been opened, place a T-tube as above.

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15.6 Cholangitis caused by ascaris Ascaris worms sometimes crawl up into the common bile

duct and gallbladder, where they can cause biliary colic,

acute cholecystitis, obstructive jaundice, cholangitis,

and pancreatitis. This most often happens when a child has

been given an antihelminthic. So, if a child has cholangitis,

or if an adult does not fit the usual clinical picture for

biliary disease, suspect ascariasis. Finding ascaris ova

should arouse your suspicion, but does not confirm the

diagnosis. Get an ultrasound scan. Do not operate, except

on the indications below.

Nasogastric suction will empty the upper intestinal tract.

Systemic antibiotics will help to control the cholangitis.

Later, treat with levamisole 120mg stat, or piperazine 4g

stat, or if there is multiple parasitic infestation,

mebendazole 100mg od for 3 days, repeated after 15 days.

N.B. Dead ascaris worms may still block the bile duct!

SPECIAL TESTS. There is a microcytic hypochromic

anaemia, a leucocytosis with >50% eosinophilia; bilirubin

is raised in cholestatic obstruction and amylase in

pancreatitis. Ascaris lumbricoides eggs can be found in the

stool.

ULTRASOUND is best to determine if the ascaris worm

is no longer in the bile duct (38.2B).

INDICATIONS FOR SURGERY. Deepening jaundice,

spiking fever, chills and rigors which do not respond to

antibiotics; nausea and vomiting, toxaemia, dehydration,

tachycardia, and perhaps hypotension; together with a

leucocytosis. If there are these symptoms, explore and

drain the bile ducts (choledochostomy, 15.5) after

appropriate preparation. Remove any worms you find.

Avoid a sphincterotomy as ascaris may then more easily

crawl into the pancreatic duct subsequently.

15.7 Other causes of cholangitis

(1).In East Asia, liver flukes, opisthorchis, found in fish

and snails, are extremely common. Many thousands of

flukes can live for many years in the bile ducts causing

inflammation. Resulting fibrosis leads to stricturing and

dilation, secondary bacterial infection and stone

development. Recurrent cholangitis can lead to biliary

cirrhosis, liver failure, hepatorenal syndrome, portal

hypertension or septicaemia, as well as pancreatitis.

Recurrent inflammation may result in cholangiocarcinoma,

and chronic infestation can lead to a salmonella carrier

state if secondarily infected.

Presentation is usually at 20-40yrs (males more

commonly), initially with non-specific malaise but then

with a high swinging fever, chills, and rigors, a gnawing

right upper abdominal pain, and mild jaundice (Charcot's

triad), usually with a history of previous attacks.

The liver is tender and enlarged and the gallbladder may

be palpable. The urine is dark, but the stools are seldom

clay-coloured; complete obstruction of the common bile

duct is rare.

(2).Around the Mediterranean, in East Asia, Latin

America, sheep liver flukes, fasciola hepatica, are found.

These flukes are large and tend to remain in extrahepatic

bile ducts. The flukes may actually eat into the wall of the

ducts, which leads to haemobilia, presenting as

haematemesis and melaena, or more rarely perforate the

duct causing peritonitis. Inflammation leads to similar

complications as with opisthorchis, but because the extra-

hepatic ducts are preferentially involved, gallbladder

distension and empyema are more common

(3).Primary sclerosing cholangitis is an inflammatory

condition affecting both intra- and extra-hepatic bile ducts,

in men and women equally of 25-40yrs. Fatigue, weight

loss, right upper abdominal pain, intermittent jaundice and

itching are usual; an acute attack of cholangitis is rare.

A similar picture can arise in HIV disease (5.6), with or

without papillary stenosis. No medication has been found

helpful.

(4).Rupture of a hepatic hydatid cyst into the bile ducts

(15.12).

SPECIAL TESTS.

There is a leucocytosis (and eosinophilia with fluke

infestation); the serum bilirubin and alkaline phosphatase

are raised. If infection is severe and liver cells are

involved, the transaminases are raised. Measure the serum

amylase, because there is a 10% chance that there is also

pancreatitis. You may find ova and dead flukes in the

faeces and in duodenal aspirates.

RADIOGRAPHS.

A plain radiograph may show air in the biliary tract due to

an incompetent sphincter of Oddi.

ULTRASOUND often shows dilation of intra-hepatic

before extra-hepatic ducts, and may actually detect mobile

flukes (38.2B).

NON-OPERATIVE TREATMENT.

If the disease is mild, take blood cultures and treat with

antibiotics (cefradine or gentamicin, 2.8). Add vitamin K

10mg IM. Start intravenous fluids, restrict oral fluids and

aspirate the stomach through a nasogastric tube.

Praziquantel 25mg/kg tid for 2days is the most effective

treatment for opisthorchis but is ineffective against

fasciola, for which bithionol 1g tid alternate days for

5days is 100% effective.

INDICATIONS FOR OPERATION.

(1) Failure of non-operative treatment.

(2) A palpable, tender, enlarged gallbladder.

(3) Septicaemia.

LAPAROTOMY. Aim to remove all biliary débris by

washing out the extra- and intra-hepatic bile ducts with

copious amounts of saline. Prepare the patient (15.5).

Perform a choledochostomy (15.5), and insert a T-tube.

In the presence of septicaemia and an enlarged gallbladder,

perform a cholecystostomy (15.3).

When acute symptoms have settled, treat any liver flukes.

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15.8 Cholecystectomy (GRADE 3.3)

Removing the gallbladder is the standard method of

treating chronic gallbladder disease, but it is not an

operation for the occasional surgeon, so unless you

are experienced, it is better to treat cholecystitis

non-operatively (15.2,3). However, if symptoms and signs

get worse, and you cannot refer the patient, and have

sufficient experience, it is best to operate early on an

acutely inflamed gallbladder than later when it becomes

hopelessly stuck down.

If symptoms persist, consider the option of

cholecystostomy (15.4) before deciding on

cholecystectomy which can be difficult and the

complications can be serious. The main dangers are

bleeding and injuring the common bile or hepatic ducts.

Do not try to remove a fibrotic, contracted gallbladder.

Unfortunately, you will not be able to predict if the

operation is going to be easy or difficult. So, be prepared

to bail out: abandon the operation, or limit yourself to a

cholecystostomy after all. We describe 2 methods of

removing the gallbladder: (i) the retrograde in which you

first dissect and tie its neck, and (ii) the antegrade in which

you start at the fundus.

The commonest cause of an injured bile duct or hepatic

artery is an ‘easy’ operation done quickly. Another cause

is anatomical variability (15-3).

ELECTIVE CHOLECYSTECTOMY

INDICATIONS.

(1) Gallstones causing several attacks of cholecystitis.

(2) A carrier of salmonella typhi.

CONTRAINDICATIONS

N.B. These are relative, but important:

(1) Inexperience.

(2) Uncertain diagnosis and failure to exclude other causes

of dyspepsia.

(3);Insufficient symptoms and signs which justify the

operation.

(4);Complicating factors, e.g. HIV disease or excessive

obesity.

(5);The need to bail out, or perform a cholecystostomy,

if it is too dangerous to proceed.

ANTIBIOTICS. The main cause of death in gallbladder

surgery is postoperative sepsis. Use a perioperative

antibiotic (2.9) unless the case is a completely elective

one.

PREPARATION.

A self-retaining and a Deaver's retractor are almost

essential. You will need two assistants as well as the scrub

nurse. If you have facilities for radiography in theatre,

make sure the patient lies on a suitable table so that

radiographs can be taken of the upper abdomen.

Check for sickle cell disease if this is common in your

area.

INCISION. Make a right subcostal (Kocher’s) or midline

incision (11-1) extending up to the costal margin.

The Kocher’s incision gives better access to the

gallbladder itself, but the midline incision better access to

the bile duct, and any other pathology that may be present.

Fig. 15-3 ANATOMY OF THE BILIARY SYSTEM.

A, normal relationships of structures in this region. B-F, relations of

the right hepatic artery. In B, (and A) it runs posterior to the

common hepatic duct (64%). In C, it runs anterior (24%), and in D,

it arises from the superior mesenteric artery (9%). In E, it runs

anterior to the portal vein (91%) and in F, posterior (9%).

G-L, variations in the bile passages (>50%). Note the accessory

hepatic ducts in positions of surgical danger. M, a small pouch

(Hartmann's pouch) may project from the right wall of the neck of a

diseased gallbladder downwards and backwards towards the

duodenum. When it is well marked the cystic duct arises from its

upper left wall and not from what appears to be the apex of the

gallbladder.

(1) fundus of the gallbladder. (2) neck of the gallbladder. (3) cystic

duct. (4) common bile duct. (5) common hepatic duct. (6) right

hepatic duct. (7) left hepatic duct. (8) portal vein. (9) right branch of

the portal vein. (10) left branch of the portal vein. (11)porta hepatis.

(12) aorta. (13) some fibres of the diaphragm. (14) coeliac artery.

(15) left gastric artery. (16) splenic artery. (17) right gastric artery.

(18) gastroduodenal artery. (19) hepatic artery. (20) right hepatic

artery. (21) left hepatic artery. (22) Hartmann's pouch. (23) cystic

artery. (24) epiploic foramen (entrance to the lesser sac).

After Basmajian JV, Grant's Method of Anatomy, Williams & Wilkins 9th

ed 1975 with kind permission.

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Feel for the gallbladder. Feel for stones in the gallbladder

and in the bile ducts. Feel both lobes of the liver to be sure

they are smooth and normal. Examine the stomach and

duodenum. Feel the pancreas.

If the gallbladder seems far up under the rib cage,

run your hand over the right lobe of the liver, divide the

falciform ligament across the dome of the liver, and draw

it down. Put some large packs between the diaphragm and

the liver - do not forget to remove them afterwards!

Insert a self-retaining retractor, and try to see the

gallbladder. Get the anaesthetist to empty the stomach with

a nasogastric tube. Use long tissue forceps to place large

moist abdominal packs over the hepatic flexure of the

colon, the duodenum, and the stomach. Ask your first

assistant to draw these downwards and medially.

You should now be able to see under the liver clearly.

Protect the liver with a pack, and ask your second assistant

to retract it upwards and laterally with a large Deaver's

retractor (15-4B). Look at the gallbladder. Divide any

omental adhesions to the gallbladder, if present.

If the gallbladder is acutely inflamed, perform a

cholecystostomy (15-1).

If it is very small, shrunken, thick-walled, contains

stones, and is firmly stuck to nearby structures, leave it

alone, or take out the stones and perform a

cholecystostomy. Removing such a gallbladder will be

very difficult.

If it looks and feels reasonably normal, apart from a few

stones, and is attached by fine adhesions only, it should be

safe to proceed.

A. THE RETROGRADE (‘DUCT FIRST’) APPROACH.

Use this if you can readily find the cystic duct, the

common bile duct, and the hepatic artery, in the free edge

of the lesser omentum. The epiploic foramen (of Winslow)

lies behind it; you should be able to pass one or two

fingers through it into the lesser sac.

Place a gallbladder clamp, or sponge-holding forceps on

Hartmann's pouch (15-4C). This is a widened area in the

lower part of the patient's gallbladder, just before it tapers

off into the cystic duct. Pull gently upwards on these

forceps, so as to stretch the tissues and make dissection

easier.

Incise Calot’s triangle of peritoneum between Hartmann's

pouch and the common hepatic duct. This will appear

when you apply traction to the sponge-holding forceps on

Hartmann's pouch. It is a most important step. Start by

making a small nick in the peritoneum with a long pair of

Metzenbaum scissors. Carefully insert the tips of the

scissors, then, using 'the push and spread technique' (4-9),

or a Lahey dissecting swab, open up enough of the

patient's peritoneum to expose the deeper structures.

CAUTION! Be careful not to cut any small blood

vessels. Bleeding will make the operation difficult.

By spreading the blades of the scissors (but not too far!)

before you cut, or using a Lahey dissecting swab, you

should be able to separate peritoneum only.

Take a Lahey swab (15-4C,E), and gently push apart the

peritoneum, so that you see the junction of the common

bile duct, hepatic and cystic arteries. This is most

important. Do not proceed unless you are certain of the

anatomy!

CAUTION! There are some important anatomical

variations:

(1) The common bile duct and the cystic duct may join

high or low (15-3G-L). The cystic duct may be very short

and the common bile duct is then dangerously tented by

traction on the gallbladder.

(2) The right hepatic artery may pass behind the common

hepatic duct (15-3A, B, more common) or in front of it

(15-3C, less common).

(3) The cystic artery may be closely bound to the common

hepatic duct.

(4) The cystic artery usually (64%) arises from the right

hepatic artery. It may cross behind (usually) or in front of

(unusually) the common hepatic and cystic ducts to reach

the gallbladder. Sometimes, it arises from the common

hepatic (27%) or the left hepatic artery (5%), or from other

arteries in the region (rare).

Be sure of your landmarks before you start to divide

anything. Use a Lahey swab and dissect by the 'push and

spread' method and thereby find the junction of the

patient's cystic and common bile ducts, as described

above. Be sure to identify 2cm of the common duct, both

proximal and distal to the junction. This will give you an

idea of its course and direction. The common bile duct lies

to the right of the structures going to the porta hepatis, and

is a greenish colour: identifying it is one of the keys to safe

gallbladder surgery.

If the cystic artery runs posterior to the common

hepatic and cystic ducts (usual), take extra care. Using

traction with your left hand on the gallbladder, follow the

cystic artery onto the gallbladder. Do not expect to feel any

pulsation in such a small vessel. If a strand of tissue runs

to the gallbladder, assume it is the cystic artery, pass

2 mounted ties around it, and divide between them. Expect

to find other branches and deal with them in the same way.

If the cystic artery runs anterior to the common

hepatic and cystic ducts (unusual), define it by blunt

dissection, and make sure that it is indeed going to the

gallbladder.

CAUTION! Do not tie the right hepatic artery by

mistake.

If you are sure you have found the cystic artery,

tie it doubly proximally and then close to the gallbladder

with 2/0 silk (15-4D), and divide it leaving a short cuff of

tissue, distal to the tie.

If you have found the junction of the cystic and

common bile ducts, and you are sure that what you

presume is the cystic duct is going to the gallbladder,

and nowhere else, define it further, using blunt dissection

(15-4E). This is the time to perform an operative

cholangiogram if you can and you are still not sure.

Using a long pair of Lahey forceps, gently open up the

cleft between the cystic and common hepatic ducts.

Pass a mounted tie of '0' absorbable suture through this

cleft, and around the cystic duct, but not too close to the

junction to cause a kink there. Tie it and for safety’s sake,

tie a 2nd suture around the cystic duct (15-4F).

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Place another Lahey clamp on the cystic duct, close to

the gallbladder, above the ties. Cut the cystic duct just

flush with the Lahey clamp, leaving enough tied cystic

duct behind, so your ligature will not slip off.

If the cystic duct is very large, transfix it (15-4G).

CAUTION! Only divide and tie structures that are

passing to the gallbladder. Don’t leave too long a

stump of cystic duct behind as it may it form a stone.

You should now be able to strip the gallbladder from

its bed by pulling it gently upwards on the clamps.

Cut any peritoneal bands that join it to the liver

(15-4H), but tie off anything else: there may be a

vessel or an anomalous bile duct inside a strand.

If the bed of the gallbladder oozes, press a warm

pack into it. If small veins continue to bleed, cauterize

them. It is unnecessary and dangerous to close the

peritoneum over the bed of the gallbladder.

CAUTION! Check to make sure that the stump of the

cystic duct is secure and that no bile is leaking.

B. THE ANTEGRADE (‘FUNDUS FIRST’)

APPROACH. Use this if you cannot readily find the

cystic duct, common bile duct, and hepatic artery.

Place a gallbladder clamp or sponge-holding forceps

on the fundus of the gallbladder, and divide the

peritoneum between the fundus and the liver. You may

need to tie any larger vessels that bleed. Mobilize the

gallbladder in this way anteriorly and posteriorly,

continuing till you reach the neck of the gallbladder.

Locate the cystic duct and trace it to the junction with

the common bile duct. Then continue as above.

OPERATIVE CHOLANGIOGRAPHY (38.1)

is important if there has been a history of jaundice,

if ultrasound shows dilated extra-hepatic bile ducts

with or without showing a stone, and if a stone is

palpable in the common bile duct.

CLOSING THE WOUND. Place a soft rubber drain

through a stab wound down to the porta hepatis if

tissues are inflamed or you are not certain that the

cystic duct ligature will hold: a controlled bile leak is

better than an uncontrolled one! Close the abdominal

wound (11.8); do this in layers if you have used a

Kocher incision.

Fig.15-4 REMOVING THE GALLBLADDER.

A, incisions. B, expose the gallbladder. C, expose the cystic duct.

Note that the second forceps holds a Lahey swab. D, tie the cystic

artery. E, free the cystic duct. F, tie the cystic duct. G, if the

cystic duct is very large and thickened, transfix and tie it like

this. H, separate the gallbladder from the liver. N.B. if the liver

bed bleeds, pack it.

After Rob C, Smith R. Operative Surgery, Butterworth 2nded 1969,

Vol4, p.404, with kind permission.

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DIFFICULTIES REMOVING THE GALLBLADDER

If you find an adherent inflammatory mass around the

gallbladder, withdraw and close the wound.

Consider operating later, when the inflammation has

subsided. Rarely this is a malignant mass, which is forever

inoperable.

If you palpate stones in the common bile duct, or find

them on an operative cholangiogram, perform a

choledochostomy (15-2) and try to extract them with

Desjardin’s forceps, or perform a transduodenal Oddi

sphincterotomy (15.5). Perform a post-extraction operative

cholangiogram, if you can.

If the cystic artery bleeds from the depths of the

wound, this can be alarming. Do not clamp blindly.

(1);Insert warm moist packs, apply pressure and wait

5mins by the clock. The spurting vessel will then be easier

to find and control. Or,

(2);Put your index finger into the epiploic foramen

and squeeze the structures (portal vein, bile ducts, and

hepatic artery) in the free edge of the lesser omentum

between your index finger and your thumb (the Pringle

manoeuvre). This will control bleeding from the stump of

the cystic artery. When you have suction and instruments

ready, remove the packs and try to visualize the vessel,

and clamp it. Transfix it carefully with 3/0 silk. Do not use

diathermy in the depths of the wound especially if you

can’t see properly! If exposure is poor, enlarge your

incision.

If you suspect you have injured the cystic duct early on,

make sure your suction is working properly and aspirate

bile so you have a good view. If necessary, enlarge your

incision. Get a cholangiogram if you cannot interpret the

anatomy. If the cystic duct is incompletely divided, hold

the part near the gallbladder in a Lahey clamp, and pass a

mounted tie around it at the common bile duct end and

complete the division of the cystic duct. If you injure it

very near its union with the common bile duct, transfix it

and carefully tie it, dividing it distally. Make sure you

haven’t kinked or narrowed the common bile duct.

If you find that you have damaged the common bile

duct you will have done so in one of three ways:

(1) By a ligature or by a clamp; undo the ligature or take

off the clamp and inspect the damage. Perform a

choledochostomy (15-2) higher up, and pass a T-tube limb

inside through the damaged area.

(2) By partly dividing it; leave a T-tube threaded up and

down the duct and proceed as for choledochostomy.

Try to repair the hole in the bile duct using interrupted 4/0

absorbable sutures, taking care not to narrow it. Keep the

T-tube in for 6wks, and then get a T-tube cholangiogram

and remove it if there is free flow into the duodenum.

(3) By completely dividing it; then try to drain the bile by

passing a tube into the severed proximal end of the bile

duct and secure it. You can leave this to drain externally

into a bag. Or you can try to insert a T-tube into both ends

of the severed duct, tie it so it doesn’t slip out and manage

the T-tube as before.

If you cannot find the distal end of the bile duct,

however, insert the distal limb of the T-tube directly into

the duodenum and secure it with a purse-string absorbable

suture. (To make a permanent by-pass, the definitive

operation of choledochojejunostomy-en-Y using a Roux

loop, is a very demanding procedure.)

N.B. Learn from your mistakes, seek to be able to

forgive yourself, and carry on.

DIFFICULTIES AFTER CHOLECYSTECTOMY

if fresh blood discharges from the drain, the pulse rises,

the blood pressure falls, and there are signs of a

haemoperitoneum, the cystic artery is probably bleeding.

Reopen the abdomen, extend the incision, suck out all the

blood and insert packs to control the haemorrhage.

Then try to visualize the bleeding vessel, clamp it and tie it

off.

If bile comes from the drain, with fever, severe pain

and a leucocytosis, suspect that infected bile and exudate

are pooling under the liver. Treat with gentamicin or a

cephalosporin. Perform an ultrasound if you can to locate

and quantify the amount of liquid. If there is no

improvement, reopen the abdomen, extend the incision,

suck out all the bile and inspect the cystic duct stump.

If this is obviously leaking and you can hold it in a clamp,

transfix it. Usually the whole area is grossly inflamed

and you will not be able to identify structures easily;

make sure the area is adequately drained.

If the patient becomes jaundiced, suspect the bile duct

has been damaged or a stone has lodged in the distal bile

duct. Try to confirm this by finding a dilated proximal

biliary tree on ultrasound (38.2B). Unless you have access

to sophisticated endoscopy, arrange a re-exploration which

is difficult, and may mean a choledocho-jejunostomy-en-

Y. If you cannot manage this, you can try to drain the

proximal biliary system percutaneously through the liver

under ultrasound guidance, or insert a T-tube (15.5) in the

dilated part of the duct. Distal stones may pass on their

own; a specialized endoscopist may be able to remove

them from below.

15.9 Obstructive (cholestatic) jaundice

When jaundice is due to an obstruction in the flow of bile:

(1) The stools are pale.

(2);The urine is dark, and contains little or no

urobilinogen.

(3);The skin itches because of deposition of bile salts.

These features are most marked in complete obstruction,

as when carcinoma blocks the common duct. Pain and

fever are usually absent. Stones typically cause an

intermittent obstruction, and a less characteristic picture.

If a stone impacts in Hartmann's pouch (15.4, 15-3M) or in

the cystic duct, it causes pain but does not impede the flow

of bile down the common duct, so jaundice is absent.

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If an older patient has a steadily deepening and usually

painless obstructive jaundice, and the gallbladder is

palpably enlarged, some tumour is probably obstructing

the common bile duct.

It is unlikely that there are gallstones (Courvoisier’s rule).

This is probably incurable, but a cholecystojejunostomy to

decompress the gallbladder, by diverting the bile into the

jejunum, may make the patient’s last days more bearable.

There are several causes, however, of obstructive jaundice:

(1) A secondary tumour in the porta hepatis, usually from

a primary in the stomach or gallbladder itself.

(2) Carcinoma of the head of the pancreas.

(3) Cholangiocarcinoma or other cholangiopathies (15.7).

(4) Metastatic liver carcinoma.

(5) Hepatoma (although this is a common disease,

presentation as obstructive jaundice is unusual).

(6) Drugs, e.g. antibiotics, contraceptives, chlorpromazine,

cimetidine, oestradiol, imipramine and many others.

In endemic areas other causes are liver flukes (15.7)

or hydatid disease (15.12).

In neonates, look for a congenital abnormality (33.9)

DIFFERENTIAL DIAGNOSIS. First try to decide what

kind of jaundice the patient has.

Haemolytic jaundice. The stools are dark. There is no

bilirubin in the urine, but the urinary urobilinogen is

increased. The blood shows increased levels of

unconjugated prehepatic bilirubin (leading to high

readings on the indirect van den Bergh test). The serum

transaminases (GPT & GOT) are normal, and so is the

alkaline phosphatase. There is a reticulocytosis. Look for

evidence of a haemoglobinopathy, especially sickle cell

disease, and malaria.

Check for consumption of medicines, especially dapsone

or sulphonamides. Check for a splenomegaly and insect or

snake bites.

N.B. Haemolysis may result in pigmented gallstones!

Obstructive jaundice. The stools are pale (clay-coloured

if obstruction is complete), and show no improvement in

colour in 10days. There is bilirubin in the urine, but little

or no urobilinogen. There is a high conjugated

(posthepatic) bilirubin level (giving high readings on the

direct van den Bergh test). The alkaline phosphatase is

very high. The transaminases are usually normal.

Hepatocellular jaundice. This is commonly viral hepatitis

with an obstructive phase lasting 7-10days, but sometimes

much longer. At this stage the stools are pale.

The urine contains bilirubin but little urobilinogen.

The serum bilirubin is moderately increased (mostly

conjugated). The alkaline phosphatase is usually only

moderately increased, but if cholestasis is a prominent

feature it can rise to levels seen in obstructive jaundice.

The transaminases are increased. As the oedema of the

cells settles, the stools become normal or even dark,

the serum bilirubin falls, the urinary urobilinogen rises or

reappears, and the transaminases fall gradually. The return

of stool colour is the most important sign. This form of

jaundice is not common >35yrs.

CAUTION! You may have difficulty distinguishing the

obstructive phase of hepatocellular jaundice from surgical

obstructive jaundice. Do all you can to make the

distinction.

A laparotomy for a stone may be life saving, but GA

(especially with halothane) and the trauma of surgery may

cause hepatocellular jaundice to deteriorate, perhaps

fatally.

ULTRASOUND (38.2B) is very useful. You need to show

extrahepatic bile duct dilation >7mm to make an operable

diagnosis.

Suggesting malignancy:

(1).Relentlessly progressive steadily deepening obstructive

jaundice, weight loss.

(2).A palpable gallbladder which you can feel as an

elongated, smooth, non-tender mass, normal in contour,

and slightly mobile, which may extend to the umbilicus or

even below it. If you can feel a distended gallbladder,

it strongly suggests a malignant obstruction at the lower

end of the common bile duct, but its absence does not

exclude this. Aspiration of green bile implies free drainage

from the common hepatic duct, but aspiration of ‘white

bile’ (i.e. mucus) suggests occlusion of the cystic duct.

Suggesting metastases in the liver or a hepatoma:

a large, hard, knobbly liver. A bruit is often present with a

hepatoma, ascites is common, and is often bloodstained.

Suggesting a carcinoma of the stomach with metastases

in the porta hepatis: pain, anorexia, vomiting, an upper

abdominal mass, and the visible peristalsis of pyloric

stenosis. Anaemia is common.

Suggesting carcinoma of the head of the pancreas:

vague epigastric pain, a palpable gallbladder and weight

loss.

Suggesting gallstones: a long history of intermittent

varying jaundice, severe intermittent colicky pain, fever,

chills, and rigors (suggesting cholangitis), little or no

weight loss, flatulent dyspepsia. A leucocytosis suggests

cholecystitis.

Suggesting tuberculosis: caseating nodes in the porta

hepatis, with signs of glandular tuberculosis elsewhere.

Suggesting stenosis of the bile ducts, either malignant

or benign: a tender, enlarged liver. A chronic history of

repeated attacks of cholangitis. The gallbladder may or

may not be palpable. Common where liver flukes are

endemic.

Suggesting carcinoma of the gallbladder: an enlarged

liver and a hard, irregular mass in the right

hypochondrium, usually in a female.

MANAGEMENT. If there are gallstones, the patient needs

a choledochostomy (15-2) unless you can remove the

gallstones endoscopically. If there is malignant disease

with obstruction at the lower end of the common bile duct,

a cholecysto-jejunostomy may help unless you can refer

the patient for endoscopic stenting.

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CHOLECYSTO-JEJUNOSTOMY FOR OBSTRUCTIVE

JAUNDICE (GRADE 3.3)

INDICATIONS. In practice the presence of a smooth

enlarged gallbladder is the only clear indication to operate.

However, you may still achieve a good result in some

cases where the gallbladder is not distended.

CONTRAINDICATIONS. Cachexia, debility, a hard

irregular gallbladder mass, a hard craggy liver due to

metastatic deposits, hepatoma, a large gastric tumour,

ascites.

PREPARATION. Confirm suitability for operation by

aspirating green bile from the gallbladder (if necessary

under ultrasound control). Treat with vitamin K 10mg IM

od at least 48hrs preoperatively. This will reduce a

tendency to bleed. Patients with jaundice are prone to

acute renal failure if their glomerular filtration rate falls.

So make sure hydration is adequate preoperatively.

Treat with dextrose IV to combat hypoglycaemia when

starved pre-operatively.

Fig. 15-5 CHOLECYSTO-JEJUNOSTOMY.

A, the incision. B, the first layer of the anastomosis.

INCISION. Open the abdomen through an upper midline

incision. Expose the liver and subhepatic area (15.8).

Good exposure is essential. Inspect and feel the upper

abdominal viscera carefully. Is the gallbladder normal in

size and appearance? If it is a hard, irregular mass which is

fixed to the surrounding organs, it is probably malignant.

If the gallbladder is inflamed, or contains many stones,

perform a cholecystostomy (15.3), unless the obstruction

in the bile duct is proximal to the cystic duct junction.

Do not try to anastomose bowel to a thick walled,

inflamed, oedematous gallbladder.

Feel the pancreas, especially its head. Lift the transverse

colon upwards and forwards out of the wound with your

left hand, while you feel the pancreas at the base of the

transverse mesocolon.

Its head lies to the right of the vertebral column at this

level. A hard, knobbly, craggy mass suggests a tumour.

Also feel it from above. Stand on the left side of the table

and feel with your right hand while you pull the hepatic

flexure of the colon medially. Place your thumb anteriorly

and your fingers posteriorly. Feel the head of the pancreas

lying in the concavity of the duodenum. If necessary,

mobilize the duodenum (15.5), so that you can feel the

pancreas properly.

CAUTION! Do not biopsy the pancreas. Unless you use

special methods like fine needle aspiration you may cause

pancreatitis and a fistula. However, if there are distant

nodules, try to get tissue for histopathology.

Feel the porta hepatis and the structures lying in the free

edge of the lesser omentum. Can you feel any craggy,

fixed, indurated masses, suggesting primary carcinomas of

the bile ducts or secondary deposits? Feel the stomach.

If you find deposits suggestive of tuberculosis (16.5),

take a small biopsy of surrounding tissue.

INDICATIONS FOR PROCEEDING FURTHER:

Decide only what to do next at this stage.

If there is an enlarged and distended but otherwise

normal gallbladder, showing that there is an obstruction

in the common bile duct, proximal to or within the head of

the pancreas, with no obstruction to the cystic duct,

perform a bypass.

If there is ‘white bile’ (mucus), on aspiration from the

gallbladder, the cystic duct is obstructed and a

cholecysto-jejunostomy will be futile.

METHOD.

Pack off the distended gallbladder. Decompress it as at

cholecystostomy (15-1). Remove the purse string suture,

and extend the opening with scissors to a length of 1·5cm.

Apply Babcock clamps to the fundus of the gallbladder

about 1cm from each end of the incision. Lift the

transverse colon upwards and look for the ligament of

Treitz. This is the point where the retroperitoneal 4th part

of the duodenum emerges to become the jejunum, slightly

to the left of the vertebral column, and distal to the

attachment of the mesentery of the transverse colon.

Choose a loop of jejunum 30cm distal to the ligament of

Treitz, and draw it up towards the open gallbladder.

Apply one or two non-crushing bowel clamps across the

jejunal loop. Apply two Babcock clamps 3cm apart on the

antimesenteric border of the jejunum, to match those on

the fundus of the gall- bladder. Bring these clamps

alongside one another, making sure that there is no tension

on the jejunal loop. Aim to make a 1·5cm diameter stoma.

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CAUTION! Make the anastomosis neatly and carefully:

biliary peritonitis is a serious complication of a leak.

The end-to-side anastomosis is similar to that for a

gastroenterostomy (13.7). Make the seromuscular outer

layer of sutures of 3/0 on an atraumatic needle.

Insert 5 sutures, which should ideally pick up only the

seromuscular layer of the jejunum, but which will

probably be of full thickness, in the wall of the

gallbladder.

Place them about 2mm away from the cut edge of the

incision, and on the bowel side about 2mm back from the

antimesenteric border of the jejunum. Incise the jejunum

3mm back from the suture line. Trim away redundant

mucosa with fine scissors. Apply Babcock forceps

temporarily over any bleeding points. Insert a continuous

'all coats' posterior layer of 3/0 atraumatic absorbable

sutures, starting at one end; then continue to close the

anterior layer with the same suture. Finally, continue with

the previous 3/0 to insert an anterior layer of seromuscular

Lembert sutures. Cover the anastomosis with a layer of

omentum, and suture this in place.

Be careful to close the abdominal wall soundly (11.8.)

DIFFICULTIES WITH CHOLECYSTO-JEJUNOSTOMY

If you do find gallstones, make sure that the jaundice is

not caused by stones distally in the bile duct.

If it is, perform a choledochostomy (15-2), extract the

stones, and if you are experienced, remove the gallbladder

also. If the gallstones seem an incidental finding, the

gallbladder is not inflamed and there is tumour distally,

proceed with cholecystojejunostomy as above, but try to

remove the gallstones from the gallbladder itself.

If there is gastric outlet obstruction (<10% of patients),

shown by an enlarged stomach, and tumour obstructing the

duodenum, perform a gastrojejunostomy (13.7) as well.

To avoid bile refluxing into the stomach, you can make a

third anastomosis, a jejuno-jejunostomy (part of the

traditional ‘triple by-pass’) but this adds to the morbidity.

Remember you are doing palliative surgery only.

A Roux-en-Y (15.14) cholecysto-jejunostomy is probably

a better combination with a gastro-jejunostomy.

15.10 Liver abscess

A. Amoebic liver abscess:

extra-intestinal amoebiasis

When Entamoeba histolytica spreads outside the bowel,

it usually involves the liver. Here it can cause an 'abscess'

filled with liquid necrotic liver. To start with this is yellow

or yellow-green, later it becomes a syrupy dark reddish-

yellow. The central area of necrosis is surrounded by

zones of progressively less damaged tissue and amoebae.

The term amoebic 'abscess' is a bad one, because there is

no pus.

There is an 80% chance that the abscess is in the right lobe

of the liver, where you will be able to detect it clinically,

unless it is very deep. Collections in the liver are

sometimes multiple.

Metronidazole usually treats an uncomplicated liver

'abscess' very effectively, but it occasionally (if >5cm

diameter) needs aspiration, and rarely (if >10cm) drainage.

The major risk is that it will suddenly rupture into the

abdominal cavity, or through the diaphragm into the

pleural or pericardial space, or even into the lung.

Rupture into the abdominal cavity is a dramatic

catastrophe, with collapse and peritonitis, like the

perforation of a peptic ulcer.

Although the contents of an abscess are sterile, they cause

an acute inflammatory reaction in the peritoneum,

whether this is acute or chronic.

N.B. Common mistakes are:

(1) Not to perform a sigmoidoscopy.

(2) Not to recognize amoebic ulcers when you do see them.

(3) Not to remember the existence of acute necrotizing

amoebic colitis with perforation.

(4) Not to use all the evidence you can to diagnose a liver

abscess.

CLINICAL FEATURES.

The patient is usually male (8:1 chance), <30yrs, and may

be a child. In endemic areas (e.g. Kwazulu in South

Africa; Pakistan; Mexico) amoebic 'abscesses' are not

uncommon in babies, and also occur in the elderly.

The pain in the right upper quadrant, or the lower right

chest, is constant or intermittent, not colicky, and does not

radiate. It slowly gets worse, but is seldom severe.

Deep breathing and coughing often make the pain worse.

Fever, anorexia, weakness, and loss of weight steadily

progress. There is only a 30% chance of having had

diarrhoea with blood and mucus during the previous year.

Often, there is some associated disease, such as

tuberculosis, HIV, malnutrition, or alcoholism.

The liver is tender, smooth, diffusely enlarged,

and without an obvious lump. Palpation of the liver may

cause much distress. Pressure over the lower 5 ribs in the

right anterior axillary line is painful. Examine also for

evidence of a pleural effusion.

SPECIAL TESTS. Leucocytosis & anaemia. Raised ESR.

Check for hypoglycaemia & hyponatraemia.

Look for amoebic ulcers with a sigmoidoscope.

You are unlikely to find amoebae in the stools.

Use new PCR tests which are very sensitive if you can.

CHEST RADIOGRAPHY. Look for a pleural effusion,

and elevation of the right dome of the diaphragm.

ULTRASOUND is by far the most reliable diagnostic tool.

Look for a fluid-filled cavity in the liver (38.2A). Measure

how near the abscess is to rupture: <1cm liver tissue is

dangerous! You cannot differentiate an amoebic from a

pyogenic liver abscess except by aspiration.

DIFFERENTIAL DIAGNOSIS includes:

(1) hepatoma,

(2) cholecystitis,

(3) hydatid cyst,

(4) pyogenic liver abscess,

(5) perinephric abscess.

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Suggesting a hepatoma (15.11): a hard nodular mass,

liver less painful and less tender, no fever or low fever

(fever only occurs with very rapidly growing tumours),

a bruit, bloody ascites.

Suggesting cholecystitis (15.3), perhaps with spreading

suppuration: pain and tenderness is localized to the

gallbladder region, there may be a history of intolerance to

greasy foods, and presence of jaundice, more commonly in

a female.

Suggesting a hydatid cyst (15.12): the mass arises from

one or other lobe, rather than enlarging it diffusely;

it grows slowly and is largely asymptomatic; it is smooth,

tense, and cystic; tenderness is minimal, there is no fever,

and the general condition is good. All this may change

rapidly, if the cyst becomes infected.

Suggesting a pyogenic liver abscess: a short history;

severely ill with a spiking fever.

Suggesting a perinephric abscess (6.15): the swelling is

low down over the liver on the right; the distinction may

be very difficult. Aspiration may establish the site.

MEDICAL TREATMENT FOR HEPATIC AMOEBIASIS:

metronidazole 800mg tid for 5days, and then

diloxanide furoate 500mg (children: 20mg/kg) tid for

10days or chloroquine 600mg od for 5days.

ASPIRATION FOR LIVER ABSCESS (GRADE 1.4)

INDICATIONS.

(1);To confirm the diagnosis.

(2);As a method of treatment if the abscess is >5cm

diameter, or if the patient fails to improve with medication

in 48hrs, or if the abscess is in the left lobe of the liver,

as this may perforate into the pericardium.

(3);If there is on ultrasound scan <1cm liver tissue

between the abscess and the liver surface (38.2A).

(4);If there is jaundice, suggesting involvement of the

biliary system.

METHOD. Treat with metronidazole for 48hrs before

aspirating. Check the prothrombin index if there is

jaundice; and correct a clotting defect with vitamin K

10mg IM. Using LA and full aseptic precautions,

preferably under ultrasound guidance, pass a wide-bore

(>1mm) long needle on a 50ml syringe, or better, a wide

bore pigtail catheter through healthy skin, over the site of

greatest swelling, or maximum tenderness.

If you obtain >250ml, introduce a multi-holed plastic

catheter on a trocar in the same direction, attach a 3-way

tap, and aspirate until the cavity is apparently empty.

Irrigate through the tube daily. Continue until the cavity is

empty and then remove the tube.

You have only c.10% chance of finding amoebae in the

fluid. They are more often found in the wall of the cavity.

OPEN DRAINAGE FOR LIVER ABSCESSES

(GRADE 2.4)

INDICATIONS. (This is rarely necessary if you have used

metronidazole, and aspirated the abscess adequately.)

(1) A deep-seated amoebic liver abscess which you have

not been able to aspirate, and the patient is deteriorating on

medical treatment.

(2) Fluid too thick to aspirate.

(3).Very large abscesses >10cm diameter, which recur

after repeated aspiration.

(4).A large abscess in the left lobe which may perforate

into the pericardium.

(5).Abscesses causing marked elevation of the diaphragm.

(6) Secondary infection of the abscess.

(7);A suspicion of a pyogenic liver abscess or an infected

hydatid cyst.

DRAINAGE. Make a subcostal incision, pack away the

rest of the abdominal contents and insert an aspirating

needle directly into the abscess cavity, to identify it.

Push an artery forceps into it, open it and suck out the pus.

Take some scrapings from the wall of the abscess,

and examine a warm wet specimen for trophozoites.

If there is much discharge, insert a tube drain, and bring

this out through a separate incision on the abdominal wall.

The liver may recede from the abdominal wall as you

drain it, and end up as a shrunken blob, in the right upper

abdomen. Remove the drain in 6-7days, to minimize the

risk of secondary infection.

DIFFICULTIES WITH EXTRAINTESTINAL AMOEBIASIS

If there is a sudden pain like a perforated peptic ulcer,

the abscess has probably ruptured into the abdominal

cavity. Resuscitate with IV fluids and start IV

metronidazole. As soon as the general state is satisfactory,

perform a laparotomy.

Make a midline incision. Explore the liver, as best you

can, and look for the site of the rupture: a ragged area with

chocolate-coloured fluid pouring from it. Suck out as

much of this you can. Mop up what you cannot aspirate.

Irrigate all the crevices of the peritoneum with several

litres of warm saline or water. Ensure a thorough lavage,

and close the abdomen. Treat postoperatively as peritonitis

(10.1)

If there are tender ill-defined masses in the abdomen,

suspect that the abscess has leaked into the abdominal

cavity. Start intensive medical treatment, and monitor the

abdomen closely. Mark the outline of any mass, and check

its size regularly. Perform a laparotomy if it gets bigger.

If an abscess presents on the chest wall, it will ultimately

rupture through the skin, which may become infected

with amoebae, and form a chronic ulcer (14-5A).

Treat with metronidazole.

If a severe cough and dyspnoea develops, this may, or

may not, mean that there is a pleural effusion.

If the effusion is small, it will resolve as the liver abscess

improves. If it is large insert an underwater seal chest

drain.

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If there is an ulcerating skin lesion round a sinus from

the liver, caecum, or anus, remember the possibility of

CUTANEOUS AMOEBIASIS. Metronidazole cures

cutaneous amoebiasis so fast, that you can use it as a

diagnostic test. In the perianal area ulcerating skin lesions

are usually non-specific. Untreated the lesions spread fast;

biopsies show up the trophozoites.

N.B. Tuberculosis, malignancy, and fungi are often

commoner.

If the patient coughs up dark reddish-yellow fluid,

the liver abscess has ruptured into a bronchus.

Although this may drain the abscess, it may also fatally

flood the bronchial tree. Get a chest radiograph and treat

with IV metronidazole, aspirate the liver abscess,

and use postural drainage for the lung (11-24).

If the liver abscess discharges into the pericardium,

it usually does so from an abscess in the left lobe.

Pericardial rupture is not uncommon in endemic areas, is

often not recognized, and is usually fatal. Watch therefore

for abscesses in the left liver lobe, and aspirate them.

Try to aspirate the pericardium (9.2).

If there is no adequate response (<5%) to metronidazole

alone, treat with chloroquine 600mg loading dose and

150mg bd for 21days, and if necessary, dehydroemetine

65mg od IM for 10days. This drug is cardiotoxic, so you

cannot use it in heart failure.

If an epileptic fit ensues, there may be cerebral

amoebiasis. If there are no focal neurological signs, treat

with diuretics and steroids, as well as second-line therapy;

if there are, suspect a brain abscess.

B. Pyogenic liver abscess

A large pyogenic liver abscess is usually much less

common than an amoebic ‘abscess’. Organisms spread

mostly from the biliary tract, or via the portal vein from

the bowel (e.g. appendix abscess or intestinal salmonella

carried with chronic Schistosoma mansoni infestation or

HIV disease) or via the hepatic artery from a remote focus

(e.g. pyomyositis). Multiple small abscesses can result

from staphylococcal septicaemia or ascending cholangitis.

Occasionally the abscess may arise from penetrating

trauma, or infection in a hydatid cyst (15.12).

The history is usually shorter than with amoebiasis.

Jaundice suggests infection from an obstructed bile duct.

Although signs of a large abscess are like those of the

amoebic variety, much more commonly there is a fever of

unknown origin. Ultrasound is the easiest way of making

the diagnosis, and aids in liver aspiration.

Until cultures are available, use broad spectrum

antibiotics: metronidazole, gentamicin, cloxacillin and

ampicillin.

Try to aspirate the abscess completely; if you fail, proceed

to open drainage (as above). Open a large abscess to

prevent rupture into the abdominal cavity!

Test for sickle cell disease and schistosomiasis, if these are

common in your area.

15.11 Hepatoma (Hepatocellular carcinoma)

Hepatoma is the one of world's common malignant

tumours, mostly because it is so common in China,

Southeast Asia, the Amazon region and Peru, Sub-Saharan

Africa, where it is even more common than secondary

tumours of the liver. In Africa, there is a 90% chance that

a liver with a hepatoma is also cirrhotic, due to the strong

association of hepatoma with hepatitis B, C & D infection,

and with the aflatoxin produced by the aspergillus fungus

growing in damp stored food. Prevalence of hepatitis B is

also high in Greenland, Alaska and Northern Canada, and

hepatitis C is a global problem.

A hepatoma often arises simultaneously as multiple

nodules in many parts of the liver. Sometimes, a huge

mass deforms one lobe. The other primary liver tumour,

cholangiocarcinoma, is a problem in Southeast Asia.

The patient is usually male (8:1), and 30-50yrs.

He complains of pain, anorexia, weight loss, or a mass;

jaundice is a late sign. The pain is usually constant, and

sharp or burning, and is in the upper abdomen, usually on

the right.

Fig. 15-6 HEPATITIS B, C AND HEPATOMA.

The geographical distribution of the hepatitis B virus, based on

incidence of HbsAg in blood samples, correlates with hepatoma

incidence. Hepatitis C has a much broader spread in the world.

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It is commonly made worse by food, which causes an

inappropriate feeling of fullness after only a small meal.

Typically, the pain is made much worse by alcohol;

so much so that it may have caused abstinence.

Usually, presentation is late with a large, or even a huge,

firm, irregular, tender liver. Quite a small tumour may

cause prostration but normal activity may continue with a

large tumour. There may be cachexia, but not always.

Look for ascites and a large spleen.

Look for collateral veins running vertically over the

anterior costal margin, or parallel to the spinous processes.

Listen over the tumour for a bruit or friction rub; this may

be intermittent, so listen on several occasions.

If there is any room for doubt, do all you can to confirm

the diagnosis. Several diseases present as swellings of the

upper abdomen. Try to distinguish those you can treat,

such as liver abscesses, hydatid cysts, and tuberculosis,

from those you can only palliate.

The best and most non-invasive tool by far is an

ultrasound: do all you can to get such a machine and get

acquainted with it (38.2A). If you have any hope of

sending specimens for cytology, use this method.

Otherwise you need to biopsy the liver to get histology.

This can be dangerous, so use ultrasound guidance if you

can. If you cannot get histology, aspiration with a fine

needle may still be useful to detect pus or tuberculosis.

In children the primary liver malignancy is

hepatoblastoma. Usually the child is severely anaemic.

The liver may rupture with a minor injury. Chemotherapy

is the only option.

SPECIAL TESTS. Serum α-fetoprotein >500μg/l is

present in 70-80% of cases. Though this test is unlikely to

be available locally, it may be easier to get a laboratory to

do it rather than get histology on a potentially dangerous

liver biopsy. The bilirubin rises late, and is often not raised

on presentation. If it is >40μmol/l, life expectancy is

weeks only. The bilirubin and alkaline phosphatase levels

rise parallel with one another. The transaminases are

normal, unless there is also chronic active hepatitis.

If there is ascites, aspirate a sample of the fluid and

examine it. Blood-stained fluid supports the diagnosis of

malignancy, not necessarily of the liver. Anaemia is

seldom a marked feature.

Do not forget to test the bleeding and clotting times.

RADIOGRAPHS. Chest radiography usually shows that

the right lobe of the diaphragm is raised. Metastases rarely

show up but are present in 50% of patients post mortem.

ULTRASOUND is extremely useful and will show

solitary or multiple lesions, or fluid cavities (38.2A).

Use it to help guide a needle biopsy.

NEEDLE, liver biopsy, Menghini, 1∙6mm, normal Menghini point, with

adjustable stop. NEEDLE, liver biopsy, Vim-Silverman, adult size, 23mm x 88.5mm, with

Franklin modification.

NEEDLE BIOPSY OF THE LIVER (GRADE 1.4)

INDICATIONS.

An enlarged liver when the diagnosis is unknown.

Fig. 15-7 LIVER BIOPSY NEEDLES.

A, Menghini needle. This has a sharp stout end (a), with an

adjustable guard (b), and a Luer lock (c). B, viewed in cross section,

the assembly has an obturator outside the needle, and a blocking pin,

which slips loosely inside the needle and prevents the biopsy

fragment from falling back, and breaking up in the syringe.

To take a biopsy using a Menghini needle: (1) insert it through the

skin, (2) expel skin fragments, (3) aspirate, (4) advance the needle

into the liver, with the patient holding his breath, and gently suck up

tissue by holding the syringe steady, (5) extract the needle whilst

gently maintaining suction.

After King M. Medical Care in Developing Countries, OUP 1967.

(A) MENGHINI NEEDLE Fit the Menghini needle to a well-fitting 10ml syringe, set the guard at

about 4cm, and draw up 3ml of sterile saline. Pass the needle point

through the anaesthetized track through the intercostal space. Inject 2ml

of saline to clear the needle point of any skin fragments.

CAUTION! Now, ask the patient to hold his breath in expiration.

Start to aspirate, and while continuing to aspirate, rapidly push the needle into the liver perpendicular to the skin, then, immediately pull it out

again. Apply pressure to the site of the biopsy. Continue aspirating until you have placed the needle point under some saline in a glass dish.

Discharge the saline remaining in the syringe. The biopsy specimen will

appear. Rescue it and transfer it to formol saline. Clear the needle with the obturator.

(B) VIM-SILVERMAN NEEDLE. Fit the inner obturator into the sheath. With firm, but well-controlled

pressure, push the needle through the abdominal wall while the patient

holds his breath. You will feel the peritoneum 'give' as you go through it. Do not push the needle in too far at this stage. Ask the patient to take a

deep breath. If the needle moves with respiration, its tip is already in the

liver; if not, ask him to hold his breath again, and gently push it 3cm further in, or until it moves.

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This has hollowed-out biopsy jaws, a sleeve which fits over them, and an obturator to discharge the specimen. The inner jaws grasp a core of

tissue, after which you slide the sleeve over them to trap it. Surgeons vary

in the needle they prefer. A Menghini needle is in a patient's liver for a shorter time, so it is safer. Its disadvantage is that it is less likely to

withdraw a satisfactory specimen in a cirrhotic. This is important because

cirrhosis is common in areas where hepatoma is common.

CAUTION! Do not manipulate the needle during regular breathing,

or you may tear the liver. Ask him to hold his breath, then remove the inner obturator and replace it

with the biopsy jaws. Steady the needle with your left hand, and push the

jaws with your right hand into the needle as far as they will go. Ask him to hold his breath again. Hold the biopsy jaws firmly with your

right hand, and slide the outer jaws 3cm further into the liver.

This will wedge the jaws and the tissue firmly in the outer sheath. Rotate the needle once or twice, to break off any tissue which is attached

at the tip, and then quickly withdraw it. Ask him to breathe again.

You can do everything in a few seconds. Long breathholding is unnecessary. Slide the sheath over the biopsy jaws and open them. Use a

fine needle to remove the core of tissue from the jaws into formol saline.

CONTRA-INDICATIONS.

(1);Do not do this if your histology service is dubious in

quality, or if the results are unlikely to arrive for weeks!

(2);Deep jaundice, severe anaemia, or any bleeding

tendency, as shown by petechiae, ecchymoses,

or haemorrhages.

(3);Hydatid disease, where needle biopsy may lead to fatal

anaphylaxis or dissemination.

(4);Do not attempt this if you cannot transfuse blood in an

emergency. Correct coagulation problems first!

CAUTION! Measure the bleeding time (normal

<3mins) and clotting time (normal <8mins) before taking a

biopsy and treat with vitamin K 10mg IM till the bleeding

& clotting times are normal.

ANAESTHESIA. Use LA in an adult; a child may need

ketamine.

METHOD. Before you use either needle for the first time,

try it out by doing the biopsy on a mango (for example),

and if possible practise on a cadaver.

CAUTION! To avoid tearing the liver, tell the patient to

hold his breath when you are pushing the needle in,

pushing it in further, or pulling it out. There are also times

when you will want him to breathe deeply to check the

position of the needle. Before you start, make quite sure

that he understands what is being done. If you are using

LA, get him to practise holding his breath.

This is important, because you must perform the puncture

itself while he holds his breath at the end of expiration.

Lay the patient supine near to the right side of the bed,

and place a firm pillow against the left side in the hollow

of the bed. Place his right arm behind the head, and turn

his face to the left.

Choose a point in the mid or anterior axillary line in the

8th, 9th, or 10th intercostal spaces, or over the palpable mass

that you want to biopsy. Clean the skin with iodine, and

anaesthetize the chosen site with LA solution, down to the

parietal peritoneum.

Pierce the anaesthetized area with a scalpel (or with the

special trocar).

If you have not succeeded, try again in a different place.

If you fail after several attempts, there is probably no solid

tissue that can be biopsied. If the needle goes in without

any resistance, attach a 20ml syringe to it and aspirate:

you may withdraw pus of a liver abscess (15.10), or blood

from a haemangioma, or clear fluid of a hydatid (15.12).

POSTOPERATIVELY, (both methods), keep the patient

supine for 12hrs. Monitor the pulse and blood pressure

during this time, just in case there is bleeding into the

peritoneal cavity. A hepatoma is very vascular, and

occasionally bleeds when you biopsy it.

DIFFERENTIAL DIAGNOSIS. Try to exclude treatable

diseases. Some of these are inflammatory, and so produce

fever, but this also occurs in primary hepatoma (8%), so it

is not a reliable guide.

Fig. 15-8 LIVER SEGMENTS.

Each side of the liver is divided into 2 sectors: paramedian and

lateral. N.B. The falciform ligament dividing the liver into traditional

right and left lobes, does NOT equate with the right and left vascular

divisions. Each of the 4 sectors on each side are further divided

superiorly & inferiorly, hence forming 8 segments. However the left

paramedian sector is not formally divided, though known often as

segments 4A and 4B (or 9). The caudal lobe is its own segment (1).

Thus a right hepatectomy consists of removing segments (5,6,7,8) and

a left hepatectomy segments (2,3,4) whilst a left hepatic lobectomy

removes only segments (2+3).

Suggesting secondary carcinoma of the liver: a hard

nodular liver, evidence for a primary tumour. In carcinoma

of the stomach there may be a separate mass, dyspeptic

symptoms, or symptoms of pyloric obstruction.

Suggesting cholangiocarcinoma: deep jaundice, no bruit,

and a liver which is less big and irregular than with

hepatoma.

Suggesting carcinoma of the head of the pancreas:

deepening jaundice, little or no pain, the absence of bile

pigment in the stools, a gallbladder which is usually

palpable, no bruit.

Suggesting amoebic abscess: fever, a smooth, diffusely

enlarged, tender liver with no obvious lumps, no jaundice;

tenderness, especially intercostal tenderness.

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Suggesting gallstones: severe colicky pain, biliary

dyspepsia, little or no weight loss.

Suggesting hydatid disease, with cholangitis: contact

with dogs, a tense, almost painless, long-standing (years),

smooth, rubbery mass, commonly in the right upper

quadrant; little weight loss, general condition good.

Suggesting a subphrenic abscess with downward

displacement of the liver: fever and an acute or subacute

illness, cough and chest signs on the right side, shoulder

tip pain on the right side.

Suggesting tuberculosis of the liver: a hard irregular

liver, often with no fever, no jaundice, pain is not marked,

especially in an immunocompromised patient. When there

is no jaundice, you cannot distinguish hepatoma and

secondary carcinoma from tuberculosis, except by needle

biopsy, which is one reason why it is so useful.

Suggesting intrahepatic stones: fever, right upper

quadrant pain, rarely jaundice in a patient in East Asia.

PROGNOSIS. Few patients survive >6 months.

MANAGEMENT. Cytokine inhibitors may palliate

usefully, but they are enormously expensive. There is little

you or anyone else can do for him, with the rare exception

of a single tumour confined to one lobe which can be

resected in specialist centres.

Try to promote hepatitis B vaccination in your area if

hepatoma is common.

15.12 Hydatid disease

The Echinococcus granulosus tapeworms in their larval

stages cause uni- or multi-locular or multiple hydatid

cysts; in their adult forms they inhabit the gut of dogs,

wolves, coyotes and foxes. Man is infested in the same

way as sheep, horses, oxen and cattle, by ingesting ova

from canine faeces (either by hand-to-mouth transfer or

from contaminated drinking water). Hydatid disease is

widespread in Turkey, Rio Grande do Sul in Brazil, as

well as Australia, North Africa & Southern Africa;

but also in Saudi Arabia, Siberia, Northern China, Japan

and the Philippines. Turkana, in north-west Kenya had the

highest prevalence, but now <4% of the population are

infected. Programmes to control hydatid infection have

been among the most successful measures of their kind.

If hydatid disease is endemic in your area, you may find

hydatid cysts in the liver (80%), spleen (7%) or the other

parts of the abdomen (14%), or occasionally in the lungs,

brain, bones, or indeed almost anywhere. If there is a

peripheral cyst, expect that there is at least one in the liver

too.

The presentation is typically of a tense, almost painless,

long-standing (years), smooth, rubbery, mobile cyst in the

upper right quadrant, with little fever or malaise,

it is probably a hydatid cyst: it may be enormous,

and there may be more than one.

A hydatid cyst usually contains several litres of clear

highly antigenic fluid under pressure. Around it there is a

thin, tough, fibrous ectocyst. Inside this, and separated

from it often by an easy plane of cleavage, is a thick,

yellowish, slimy, gelatinous endocyst, which the parasite

forms, and which tends to split and curl up on itself when

you cut it. Scolices, which are tiny, barely visible, white

granules, and daughter cysts, like grapes or soap bubbles,

float free in the fluid of the cyst.

Echinococcus vogeli, a parasite found in Central & South

America, produces multiple cysts in the liver. Likewise,

Echinococcus multilocularis, found in Central Asia,

produces multiple cysts, but also inflammatory infiltrations

that mimic tumour, and can spread to the lungs in 30%.

Fig. 15-9 HYDATID CYST OF THE LIVER.

A-F, some of the cysts you may find. C will need a thoraco-abdominal

incision. G, a patient with a single cyst. H, abdominal distension due

to multiple hydatid daughter cysts throughout the peritoneal cavity.

After Pelissier G, Goinard P, Peguilo J. Le kyste hydatique, Masson,

Niort 1960.

A cyst in the liver may rupture into:

(1) the bile ducts and cause cholangitis,

(2) a serous cavity, where it may cause a hypersensitivity

reaction, varying from urticaria to anaphylactic shock.

The diagnosis is difficult without ultrasound, and the

disease may be so rare that you forget it as a possibility.

There is hardly ever any hurry to operate, so investigate it

as fully as you can.

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Surgery is likely to be difficult, so treat it medically before

you operate or aspirate. The method of puncture,

aspiration, injection (of scolicide) and re-aspiration (PAIR)

is safer than surgery in most cases. You may be able to do

this under ultrasound control if you have had some

experience.

If you intend to remove a hydatid cyst surgically, do so

in the plane between the tissues of host and parasite: leave

the ectocyst, and do not try to remove the entire cyst intact,

unless you can do this easily, as in the ovary or spleen.

Instead:

(1);Gain access to the cyst, and pack it off, so that if any

infective hydatid fluid does escape, it will not contaminate

the peritoneal cavity; 1mL can contain thousands of

scolices.

(2) Aspirate some of the fluid, and inject a scolicide.

(3);After 10mins, aspirate as much remaining fluid as you

can.

(4) Scoop out the endocyst and the daughter cysts.

(5);Close the cavity, so that it does not leave a sinus or a

fistula.

In a child, the cyst will probably be monolocular, so that

aspirating it will not be too difficult. But in an adult,

it is likely to be multilocular, so that:

(1);the fluid will be difficult to aspirate, because the

daughter cysts block the needle, and

(2);the scolices will be difficult to sterilize, because the

scolicide cannot penetrate in to them.

The great dangers are that you will spill the fluid which

may:

(1);allow daughter cysts to establish themselves in the

peritoneal cavity, &

(2);cause anaphylactic shock. The recurrence rate is

usually at least 25%.

PREVENTION. If yours is an endemic area, do all you

can to educate the local population, especially about

washing hands; eliminating stray dogs and regularly

deworming their domestic dogs, not feeding them

uncooked offal and burning refuse from slaughtered

animals.

SPECIAL TESTS. An absolute eosinophilia is present in

30% of patients. The Casoni test gives false -ve & +ve

results in c.20% of cases, and is no longer used.

Other antibody tests, such as the ELISA test, may also

give false negatives.

RADIOGRAPHS. Take a chest film: there may also be

cysts in the lungs. A cyst in the liver may raise the right

lobe of the diaphragm. An old aborted cyst may leave a

calcified shadow.

ULTRASOUND is the best way of detecting hydatid cysts

(38.2A). A lamellated membrane, detachment of the

membrane from the cyst wall, or the presence of daughter

cysts confirms the diagnosis. You should be able to

differentiate a hydatid from a simple liver cyst by its

having a double wall.

DIAGNOSTIC ASPIRATION. Do not try to do this,

because this may make the cyst leak, and may be fatal.

Aspiration is part of treatment. Do not try to tap a hydatid

cyst merely to make it smaller.

If you are aspirating what you think is an abscess, and

you aspirate clear fluid, it is highly likely to be a hydatid

cyst. Continue aspirating to dryness, before you remove

the needle. Then inject a scolicide, wait, re-aspirate and

then quickly withdraw the needle.

DIFFERENTIAL DIAGNOSIS.

Suggesting simple liver cyst: smooth hepatomegaly,

with single cyst wall on ultrasound.

Suggesting liver abscess: fever, tender smooth

hepatomegaly, with short history of illness.

Suggesting hepatoma: irregular huge liver with ascites

and weight loss; audible bruit.

Suggesting secondary carcinoma of the liver: hard knobbly enlarged liver with weight loss.

Fig. 15-10 OPERATION FOR HYDATID CYST OF THE LIVER.

A, high midline incision. B, expose the cyst. C, isolate the cyst with

scolicide-soaked packs, and suture a tubular sheath to the pericyst.

Work within this sheath to avoid spillage. Aspirate 50% of the fluid

into a bag of scolicide. Leave the needle in place and inject 50-100ml

scolicide till it becomes tense. Tie the purse string around the

puncture site and wait for 10mins. Re-aspirate the cyst till it is

flaccid. D, then incise the pericyst and suck out the rest of the fluid.

E, remove the daughter cysts with a spoon. F, remove the endocyst

completely with sponge forceps. G, swab out the cavity with scolicide.

Partly after Rob C, Smith R. Operative surgery: Part 1: Abdomen,

Rectum and Anus, Butterworth 2nd ed 1969 p.322 with kind permission.

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TREATMENT

Treat with praziquantel 15-25mg/kg bd for 7-14days,

pre-operatively. This kills the proto-scolices. Small cysts

may disappear without surgical intervention. Albendazole

in high doses (10mg/kg od for 28days) damages the

germinal membrane and so is complementary to

praziquantel. You should therefore use both! Repeat the

dose 4 times after a rest interval of 15days. It is contra-

indicated in pregnancy. Mebendazole 600mg tid for 3wks

is an alternative, but only effective in c.40%.

Use cimetidine 400mg bd in addition.

PERCUTANEOUS ASPIRATION, INJECTION &

RE-ASPIRATION (PAIR)

Treat medically first for a minimum of 3wks.

If there is a single cyst <5cm diameter, withdraw as

much fluid as you can under ultrasound guidance through

a wide bore needle, and inject, preferably through a

T-connection piece, an equivalent volume (or slightly

more) of a scolicide (preferably chlorhexidine 0·04%,

which is safer and more effective than other scolicides

such as cetrimide, 70% alcohol, 1% povidone iodine, 0·5%

silver nitrate, hydrogen peroxide or hypochlorite.)

Start slowly by injecting a small volume; if there is any

pain, abandon the procedure. If not, continue, and

re-aspirate after 1hr.

CAUTION! Do not use formalin or hypertonic saline as

scolicides.

Do not use PAIR if the cyst communicates with the biliary

tree. Remember that the liver moves with respiration and

so even then a needle will not stay immobile.

LAPAROTOMY FOR HYDATID CYSTS OF THE LIVER

(GRADE 3.4)

INDICATIONS.

Large, symptomatic, subcapsular cysts in young patients;

large especially peripheral viable cysts, prone to traumatic

rupture.

Do not attempt operation if the cyst is high on the right,

under the diaphragm, or there are multiple, deep-seated

cysts, or if there is a communication with the bile ducts

because extensive mobilization of the liver will be

necessary.

PREPARATION. Kill the hydatids and make

dissemination less likely by using praziquantel or

albendazole as above.

Treat with hydrocortisone 100mg IM 12hrs before the

operation, so as to minimize the danger of anaphylaxis

when you open the cyst and reduce the risk of laryngeal

spasm.

Have ready: An aspirator, or a large-bore syringe with a

needle and 3-way tap; a long pair of sponge forceps,

and a sterile kitchen spoon to scoop out the cyst; coloured

packs which will let you to see the brood capsules and

scolices more easily (soak the packs in scolicide);

2 suckers, one for the trocar (if you use one), and another

ready for any spills; a sterilized 6x15cm tubular polythene

sheath; & a scolicide.

INCISION.

Make a midline incision unless the cyst is very peripheral.

If necessary, extend this laterally in a J-shape, so that you

have adequate exposure. Another way of getting better

access is to stuff packs, soaked with scolicide, into the

right subphrenic space, so as to push the liver down.

If you know exactly where the cyst is, a subcostal incision

may be even better.

The cysts present as smooth white swellings. Look and

feel carefully to find how many there are. The rest of the

liver is usually large, smooth, and distended.

Select a place where the cyst is close to the surface,

and isolate it with carefully placed scolicide-soaked packs.

Suture a tubular polythene sheath 6x15cm with 3/0 silk to

the pericyst without puncturing the cyst. Aspirate through

the polythene sheath at least half the fluid with a 1∙5mm

needle (15-10C).

If the needle blocks, clear it by injecting a little scolicide.

If needle aspiration does not work, use a trocar and

cannula. If necessary, try introducing a multi-holed

catheter through the cannula. This will however increase

the risk of spillage. If many daughter cysts block the

sucker, it is probably multilocular.

Collect the fluid in a bag containing an excess of scolicide.

Do not use an open dish as fluid may spill! Keep a record

of the volume you withdraw, as a guide to how much

scolicide you will need to inject. Leave the needle in place

and inject 50-100ml scolicide back into the cyst until it

becomes tense. Then tie a purse string suture snugly round

the puncture site, and remove the needle. Wait for 10mins

for the contents of the cyst to become sterile.

Re-aspirate the cyst till it becomes flaccid and open it

through the part which presents most easily. Insert the tip

of the sucker, and suck out the remaining fluid. Record-

sized cysts have had over 40L! Using a kitchen spoon,

remove all the daughter cysts, sediment and debris

(15-10E). Then, using finger dissection, find the natural

plane of cleavage between the ecto- and the endo-cyst.

To get adequate exposure, you may have to incise the cyst

across the full width of its bulge, and deroof it.

Remove the yellow laminated membrane of the endocyst

completely, piece by piece, with sponge forceps (15-10F).

There will be little bleeding.

CAUTION!

(1);Try not to rupture the daughter cysts as you remove

them, because their contents are probably still infective.

(2) Do not try to remove the ectocyst; it is tightly stuck to

the liver, and will bleed.

Swab the inside of the cyst with packs soaked in scolicide,

and explore it for secondary cavities. If you find any,

repeat the process of aspiration and injection.

If the cavity is small, you may be able to bring its edges

together with mattress sutures.

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If the cavity is large, you can:

(1).Suture any obvious small bile duct openings, and leave

it alone, which is probably the wisest method.

(2).Fill it with ordinary 0·9% saline, and suture it.

(3).Saucerize it by excising the protruding portion.

The difficulty with this is that the cut surfaces of the liver

will bleed.

(4).Fill it with a graft of omentum. Dissect a strip of

omentum on a vascular pedicle and stitch this into the

cavity. The omentum will swell to fill the space and absorb

the fluid from the cavity.

(5).Bring the walls of the cyst together with multiple

absorbable sutures, so that the cavity is obliterated.

Drain large cavities for about 10days, especially if you

have not been able to remove all the endocyst.

CAUTION!

(1);Do not let the untreated cyst fluid spill, or daughter

cysts will form in the peritoneal cavity.

(2) If the needle hole leaks, insert a purse string suture.

If the cyst is a simple non-hydatid cyst, you can simply

de-roof it and obliterate the cavity with omentum.

Make sure you control bleeding from the cut cyst edge

with a running suture or diathermy.

DIFFICULTIES WITH HYDATID CYSTS

If there are signs of peritonism with an anaphylactic

response, shock, and dyspnoea, the cyst has ruptured into

the peritoneal cavity. Use hydrocortisone 0·5-1g IV, and

adrenaline 1:1000 1ml SC.

If the blood pressure falls alarmingly and there is no

other reason for it, the cause is probably an anaphylactic

reaction. Treat as above. Alternatively the cyst may have

eroded into a major vessel such as the inferior vena cava or

portal vein: apply pressure with your fingers and get

suction, bulldog clamps etc as for a vascular injury.

If there is generalized abdominal swelling, consider the

possibility of HYDATIDOSIS OF THE PERITONEAL

CAVITY. At operation you may find the peritoneal cavity

distended with hydatid cysts, and remove bucketfuls of

them. Try to remove as many of them as you can.

Then flood it with liberal quantities of 0·04%

chlorhexidine solution as a scolicide. Aspirate this and

then irrigate it with saline to wash out the remaining

scolicide. The surface of the bowel may be seeded with

small white nodules. Make sure you start praziquantel and

albendazole unless already started.

If there is a cyst in the omentum, try to remove it entire,

with part of the omentum. If you cannot do this, aspirate

and inject scolicide, as for the liver.

If there is a cyst in the spleen, perform a splenectomy

(15.17).

If there is a cyst in the kidney, aspirate under ultrasound

guidance, and introduce scolicide as above.

If there is obstructive jaundice, perhaps with

cholangitis, aim to drain the common bile duct (15.7).

Remove all hydatid sludge, debris, and daughter

cysts from the duct, and irrigate it thoroughly.

Drain the common bile duct with a T-tube.

If a cyst is leaking into the peripheral bile ducts,

sterilize, evacuate, and drain the cyst. An external biliary

fistula may develop, which may improve cholangitis

which is likely to be present.

If a fever develops postoperatively, the cyst cavity is

probably infected. Treat with gentamicin or

chloramphenicol.

If there are features of a liver abscess: a swinging fever,

anorexia, and increasing pain, suspect that a hydatid cyst

has become infected. Open it, saucerize it, and drain it

(15.10). Infection will have destroyed the hydatids.

If there are recurrent cysts, they will probably take

about 3yrs to develop, be multiple, and be in the

abdominal cavity. Distinguish recurrent cysts from the

manifestation of an unsuspected second cyst. Start medical

treatment.

If there are cerebral cysts also, use praziquantel in

higher doses (60-90mg/kg bd for 30days), together with

dexamethasone 4mg qid)

If a cyst is calcified and asymptomatic, leave it alone.

15.13 Pancreatitis

Both acute and chronic pancreatitis are not uncommon;

rarely a pancreatic pseudocyst (15.14) or abscess (15.15)

develop as complications. If the patient does not recover

1wk after an acute episode, suspect such complications.

Pathologically, acute pancreatitis varies from oedema and

congestion of the pancreas to its complete autodigestion,

with necrosis, haemorrhage, and suppuration. Less severe

forms may go on to form a tender, ill-defined mass in the

epigastrium.

The main symptom is pain, which can vary from moderate

epigastric discomfort to an excruciating, penetrating

agony, which bores through to the back, and needs high

doses of opioids to relieve it. There is tenderness in the

epigastrium, perhaps with guarding. Vomiting, paralytic

ileus and the outpouring of fluid into the retroperitoneum

may result in severe fluid loss. If you see bruising around

the umbilicus or in the flanks, this indicates intra-

abdominal haemorrhage and means the pancreatitis is

severe.

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The underlying cause is usually:

(1) alcohol abuse (especially spirits), or

(2) gallstones (or ‘sludge’), and occasionally,

(3) ascaris worms,

(4) liver flukes,

(5) leptospirosis,

(6) HIV disease (including treatment with ARV therapy),

(7) rarely typhoid.

(8) mumps or coxsackie virus,

(9) hypercalcaemia, hyperlipidaemia,

(10) systemic lupus or cystic fibrosis

(11) trauma (including endoscopic instrumentation)

(12) drugs such as sulphonamides, thiazides, œestrogens

(13) poisons such as organophosphates

(14) tityus scorpion envenomation (in Trinidad, Brazil &

Venezuela).

You may diagnose pancreatitis clinically, or from

laboratory tests, or only when (in error) you perform a

laparotomy for an acute abdomen. Estimating the serum

amylase is not difficult, and your laboratory should be able

to do it, because you should avoid a laparotomy for

pancreatitis at all costs!

Chronic relapsing or recurrent pancreatitis is one of the

causes of a severe chronic upper abdominal pain. It is quite

common in alcoholics anywhere, and there is a calcific

type found much in Kerala and Orissa in India, but also in

Japan and sub-Saharan Africa; the pancreas calcifies and

its endocrine function deteriorates. A longitudinal

pancreaticojejunostomy is helpful if the pain is

debilitating, but this is formidable surgery indeed.

Chronic pancreatitis may also be due to tuberculosis (16.5)

ACUTE PANCREATITIS

DIFFERENTIAL DIAGNOSIS includes:

(1) gastritis,

(2) perforated peptic ulcer (13.3),

(3) acute cholecystitis (15.3),

(4) rupture of a liver abscess (15.10),

(5) strangulating upper small bowel obstruction (12.2).

SPECIAL TESTS. Serum amylase rises within hours of

the start of the pain, and remains high for about 2days.

A level of >1,000 Somogyi units is almost diagnostic.

A peritoneal tap in the right lower quadrant will confirm

the diagnosis: the aspirate may be straw-coloured, or

reddish-brown, but its amylase is always high.

In severe acute disease (Ranson’s criteria),

(1) the white count is >16000/mm³

(2) the glucose is >10mM; after 48hrs,

(3) the haematocrit drops >10%,

(4) the urea rises >10mM,

(5) the serum calcium drops <2mM,

(6) the pO2 drops <60 mm Hg with a metabolic acidosis.

Hyperglycaemia is common with chronic calcific

pancreatitis.

(The Balthazar score gives the severity of the pancreatitis in terms of the degree of inflammation and necrosis seen, but this needs contrast-

enhanced CT scanning.)

RADIOGRAPHS are not very helpful but may show

pancreatic calcification, if there have been previous

attacks; and a left pleural effusion, or distended loops of

bowel from ileus.

ULTRASOUND demonstrates oedema, and fluid

collections (or even necrosis) of the pancreas (38.2C).

You may see gallstones, and especially ‘sludge’ in the

common bile duct, or a completely different diagnosis!

TREATMENT.

If pancreatitis is mild, it will settle by a régime of

restricting oral intake, with nasogastric drainage, analgesia

and IV fluid replacement.

If pancreatitis is severe, replace fluid loss energetically

with large volumes of 0∙9% saline, Ringer's lactate, or a

plasma expander. Correct electrolyte losses. Monitor the

urinary output, the haematocrit, and if possible, the central

venous pressure. Monitor glucose; start an insulin sliding

scale. The pain may be overwhelming: treat with large

doses of opioids, supplemented by diazepam or

promethazine. Administer oxygen by mask; consider

mechanical ventilation. Prophylactic antibiotics, especially

against staph aureus are advisable. You may need blood

transfusion later.

If you are sure of the diagnosis, do not operate; but it is

better to operate unnecessarily, than not to operate on a

case of strangulated bowel, for example. The amylase

level may rise with necrotic bowel. Severe cases may

benefit from lavage with saline, via tubes which can be

inserted in the flanks under LA (13.3), but attacks tend to

recur. Formal open lavage is then better.

If you do open the peritoneum, you will know that there

is pancreatitis when you see areas of whitish-red fat

necrosis on the transverse mesocolon, or omentum, and the

exudate described above. The pancreas feels swollen and

oedematous, and may contain greenish-grey necrotic areas.

The fat necrosis may be confused with TB, so take a

biopsy. Drains by themselves do not help, but you may use

them for continuous peritoneal lavage.

If the abdomen is difficult to close, leave it open as a

laparostomy putting on a vacuum dressing (11.10, 11-20)

or make fasciotomies in the rectus sheath.

DIFFICULTIES WITH ACUTE PANCREATITIS

If you find that there are also gallstones, consider doing

a cholecystectomy (15-4) later. Do not be tempted to

remove the gallbladder in the acute phase.

If, during the course of 2-3wks, septicaemia develops,

suspect that a pancreatic abscess (15.15) is developing,

especially if there is haematemesis.

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If deterioration continues, your only chance will be to

refer to a centre where CT scanning is available:

a pancreatic necrosectomy may be life-saving.

If respiratory or renal failure develop, usually in the

first 48hrs (5-10% chance), death is likely. There is little

you can do except treating with oxygen, plenty of IV

fluids, and plasma expanders. Monitor the CVP, ventilate

mechanically, add broad spectrum antibiotics and

nutritional support.

15.14 Pancreatic pseudocyst

A large watery pancreatic exudate sometimes collects in

the lesser sac. This has no epithelial lining, hence the term

‘pseudocyst’. It usually presents >3-4wks after an

abdominal injury, or an attack of acute pancreatitis, with a

mass in the abdomen and epigastric discomfort or pain.

There may be toxaemia with fever and tachycardia, but the

degree of sickness is much less than in acute pancreatitis,

or a pancreatic abscess. The mass usually distends the

abdomen: it may extend right across the epigastrium, and

reach down to the umbilicus or beyond it. It is not usually

tender, but may be quite tense and not fluctuant if very

large. Sometimes, there are symptoms of pancreatic

insufficiency, with steatorrhoea.

You can drain the cyst into the stomach, jejunum, or

percutaneously into a bag. The correct timing of these

procedures is important because the cyst has to mature to

hold sutures. It may not do so properly in HIV disease.

Draining it is less urgent than operating on a pancreatic

abscess (15.15), and there is less chance of complications.

External drainage usually results in leakage and skin

excoriation, and should be used only as a last resort;

cystogastrostomy is simple but cystojejunostomy is the

definitive operation, and you should be able to manage this

if you are confident with bowel anastomoses.

SPECIAL TESTS. The amylase level in the cyst fluid is

grossly raised.

ULTRASOUND shows a large cyst easily, though you

may have difficulty differentiating it from a liver cyst

(38.2A,C).

RADIOGRAPHS are less useful: you can make the

diagnosis by adding oral contrast: a lateral film of barium

in the stomach will show a mass bulging into the contrast

from behind. There is gross widening of the normal

contour of the duodenum. You may see patches of

calcification in the pancreas. Or, insert a nasogastric tube

and inject 200ml of air into the stomach and take a lateral

supine view of the abdomen. In a pancreatic pseudocyst

the stomach is displaced forwards, in a liver abscess,

backwards.

DRAINAGE FOR A PANCREATIC PSEUDOCYST

(GRADE 2.4)

TIMING.

Do not operate until >6wks after an attack of pancreatitis,

by which time the cyst wall will be mature enough to take

sutures. Once a pancreatic pseudocyst is palpable it rarely

disappears spontaneously. Operate as soon as possible

after 6wks; if you leave it too long it may bleed, rupture,

become infected, or destroy much of the pancreas.

DIFFERENTIAL DIAGNOSIS includes:

(1) liver abscess (15.15),

(2) hepatoma (15.11),

(3) hydatid cyst (15.12),

(4) renal cyst or hydronephrosis (27.14),

(5) gastric outlet obstruction (13.7),

(6) Burkitt's lymphoma (17.6),

(7) abdominal tuberculosis (16.1),

(8) aortic aneurysm (35.8).

Rarely a pancreatic carcinoma can form a cyst.

Fig. 15-11 PANCREATIC PSEUDOCYST.

A, approach to the cyst through the anterior and posterior walls of

the stomach. B, suture the wall of the cyst to the posterior wall of the

stomach to control bleeding. After Maingot R, Abdominal Operations,

HK Lewis 4th ed 1961 p.557 Fig. 26, permission requested.

It may be necessary to drain the cyst earlier if it is about to

rupture, if it causes persistent intractable vomiting, or has

started to bleed.

You can drain the cyst percutaneously under LA; make

sure you put two purse strings to hold the drain and invert

the cyst around the drainage tube as for a gastrostomy

(13.9). The problems are leakage and resulting skin

excoriation. External drainage is a temporary measure if

you are unable to perform a formal internal drainage

procedure.

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CYSTOGASTROSTOMY FOR PANCREATIC PSEUDOCYST

(GRADE 3.2)

PREPARATION

In dehydration, anorexia, or toxaemia, administer IV fluids

and high calorie high protein enteral feeding for a few

days pre-operatively. Insert a nasogastric tube the evening

before operation, and wash out the stomach thoroughly.

INCISION.

Make a midline incision.

Choose an area on the anterior wall of the stomach that is

overlying the cyst. Use a knife or diathermy to start a 4cm

incision in the long axis of the stomach between

2 Babcock forceps. Enlarge it with scissors. Clamp any

briskly bleeding vessels, and retract the edges of the

incision, so that you can inspect the posterior wall of the

stomach. Suck it empty.

After opening the stomach, aspirate through its posterior

wall into the cyst. Expect to find a mildly opaque

straw-coloured, or murky brownish fluid. If so, insert a

small haemostat through the hole in the stomach into the

cyst, and open it so as to enlarge the opening to 3cm.

Suck out the fluid: expect to aspirate up to 4l.

CAUTION! Do not incise the cyst widely; it may bleed

severely.

N.B. If you aspirate fresh blood, the ‘cyst’ may be an

aortic aneurysm: stop! Get an ultrasound scan (38.2D).

If you have waited the 6wks for adhesions to form and the

cyst wall to mature, there will be no need to suture the

stomach wall to the cyst, as they will already be tightly

stuck together. But control brisk bleeding from the

stomach edge; so quickly oversew the opening all round

with a continuous interlocking haemostatic suture of 2/0

non-absorbable. Do not use absorbable suture, because

pancreatic juice digests it. When you are sure the posterior

opening in the stomach is no longer bleeding, close the

anterior opening in two layers, the first a full-thickness

haemostatic continuous layer of 3/0 absorbable sutures,

and the second a seromuscular Lembert layer of

continuous non-absorbable suture. Close the abdominal

wall in the usual way.

CYSTOJEJUNOSTOMY-EN-Y FOR PANCREATIC

PSEUDOCYST (GRADE 3.5)

INCISION. This is the definitive operation. Proceed as

above; after opening the cyst, lift up the proximal jejunum

and look at its blood supply; select a point 30cm from the

ligament of Treitz where to divide the bowel so that the

distal loop easily reaches the pseudocyst. Divide the bowel

between non-crushing clamps. You will need to divide

some of the vascular arcades in the mesentery to mobilize

the distal bowel (the Roux loop) adequately. When you are

satisfied there is no tension, make an end-to-side

anastomosis of the loop to the opening in the pseudocyst.

Then anastomose the proximal cut end of jejunum to the

right side of the Roux loop some 20cm along its length

with an end-to-side anastomosis, making sure the bowel

lies comfortably. Close any mesenteric defects carefully

avoiding damage to the fine mesenteric vessels.

Fig. 15-12 THE ORIGINAL ROUX LOOP.

A, the distal afferent (Roux) loop, which you can use to drain the

gallbladder, bile duct, pancreatic cyst, or stomach. B, the proximal

efferent loop. The small bowel has been divided at c, and the

proximal part anastomosed end-to-side at c'. Here the plan is to

anastomose the Roux loop to the gallbladder.

SIMPLE CYSTOJEJUNOSTOMY FOR PANCREATIC

PSEUDOCYST (GRADE 3.4)

INCISION. This is a simpler, but less satisfactory,

procedure. Make a midline incision. Open the lesser sac to

get access to the pancreatic pseudocyst; check that its wall

is thick enough to hold sutures. Then pack off the

abdominal contents with large swabs, open the cyst by

2cm only and drain its contents. Bring a loop of proximal

jejunum up to the cyst and make a side-to-side

anastomosis (as for a gastrojejunostomy (13-16).

POSTOPERATIVELY, restrict oral intake with

nasogastric suction for 3-4days, until flatus is passed;

then start oral fluids, followed by a soft diet.

15.15 Pancreatic abscess

This is a dangerous complication of acute pancreatitis

(15.13) or perforated duodenal ulcer. Occasionally it

results from severe pancreatic injury. A collection of pus,

necrotic tissue, and clot fills the lesser sac; it enlarges

behind the peritoneum, it expands anteriorly to obliterate

the lesser sac, and it pushes the stomach and transverse

colon forwards. It may present with a catastrophic

haematemesis.

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If the abscess develops during the course of an attack of

pancreatitis, the diagnosis is usually obvious, but it may be

difficult otherwise. So if ever a severely sick patient has an

ill-defined deep-seated epigastric mass, remember that

there might perhaps be a pancreatic abscess.

SPECIAL TESTS. The urinary and serum amylase are

usually high. Check the glucose.

ULTRASOUND. A fluid-filled cavity is seen adjacent to

the pancreas, as a pancreatic pseudocyst (38.2C).

Aspiration is difficult and hazardous, so is not

recommended.

LAPAROTOMY FOR PANCREATIC ABSCESS (GRADE 3.4)

PREPARATION. Resuscitate with adequate IV saline or

Ringers lactate. Correct hyperglycaemia with insulin.

Administer oxygen, bicarbonate and calcium in seriously

ill patients. Catheterize the bladder. Treat with gentamicin,

ampicillin and metronidazole. Cross-match blood.

Decompress the stomach with a nasogastric tube.

EXPLORATION. Make an upper midline incision from

the xiphisternum to beyond the umbilicus. Open the

abdominal cavity with care, because the mass, or the

stomach or colon, may have stuck to the abdominal wall.

You may find it difficult to know what you are seeing.

Dissection is difficult and dangerous, because the tissues

are so vascular and oedematous. Lift and free the

abdominal wall from the organs under it, and insert a

self-retaining retractor. Feel for the upper border of the

abdominal mass. Try to find a place where you can incise

it without injuring anything. This will usually be through

the lesser omentum, or better, the transverse mesocolon to

the left of the ligament of Treitz. When you have decided

where to drain, seal the area from the rest of the

peritoneum with large moist packs. Using a syringe and a

large needle, aspirate the place where there seems to be the

thinnest layer of tissue between the abscess and your

finger. Take pus for culture. If you find pus under

pressure, decompress the abscess with suction. Enlarge the

abscess so that you can insert two fingers, but don't try to

dissect further. Wash out any floating solid matter.

CAUTION! Don't disturb the necrotic pancreatic tissue

at the bottom of the abscess - it will bleed!

Place 2 catheters in the abscess cavity, and bring them out

through stab wounds. Bring one out anteriorly, and the

other as far back as possible, in the most 'dependent'

position. Use these to irrigate the abscess cavity

continuously (about 2l in 24hrs). Make a feeding

jejunostomy (11.7), because oral feeding will not be

possible for 3wks, and you will probably be unable to feed

parenterally. Feeding through a jejunostomy results in less

secretion of gastric juice than feeding through a

gastrostomy.

POSTOPERATIVELY.

Continue nasogastric suction, fluids, and antibiotics until

the temperature is normal. Chart the daily drainage output.

Don't be in a hurry to remove the drains, even if leaving

them in does seem to increase the risk of a fistula.

Allowing pus to collect again is a greater risk.

If the wound is looking fairly clean, close it by secondary

suture in 7-10days.

CAUTION! This is heroic surgery! A pancreatic

abscess carries a 30-50% mortality, and often reforms,

even with adequate drainage. If so, be prepared to

re-operate 3 or 4 times if necessary. However, if you do

not operate, death is inevitable!

DIFFICULTIES WITH PANCREATIC ABSCESS

If pancreatic juice is still discharging after 2wks, leave

the catheters in situ for a month and then withdraw them

slowly 5cm per day.

If a pancreatic fistula develops, collect the juice in a stoma

bag with the orifice carefully cut to size to prevent skin

excoriation. This can be mixed with jejunostomy feeds if

malabsorption is a problem.

If bleeding becomes severe, try pinching the vessels in

the free edge of the lesser omentum between your fingers

and pack the pancreatic area. Leave the packs for 48hrs

and remove them at a second laparotomy, when bleeding

should be much less.

15.16 Pancreatic carcinoma

If the carcinoma is in the head of the pancreas (70%),

it may obstruct the common bile duct, so that presentation

is with painless progressive obstructive jaundice (15.9).

If it is in the body of the pancreas (30%), presentation is

with upper abdominal and back pain and general

symptoms of malignancy. Spread to the lymphatics and

surrounding structures is early, and 10% of patients

develop ascites.

Thrombophlebitis migrans (thrombophlebitis in any

superficial vein appearing, resolving, and then appearing

again elsewhere) may occur with any malignant tumour,

but is particularly common with this one.

Radiotherapy, chemotherapy, and surgery are of little

value, but differentiation with tuberculosis is important.

Taking a biopsy of the pancreas itself may cause

pancreatitis and worsen the condition, so try to get a piece

of tissue from an adjacent node or piece of omentum.

Sometimes carcinoma of the pancreas cannot be easily

distinguished from chronic pancreatitis (15.13)

or tuberculosis.

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15.17 Surgery of the spleen

If you operate on the spleen, you often end up removing it.

The indications for doing so (apart from trauma) must be

good, because the spleen of a tropical patient is commonly

large, and may be so firmly stuck to the diaphragm that:

(1) exposing it is difficult.

(2) bleeding is likely from the vascular adhesions that join

it to the diaphragm.

If there is portal hypertension, the vena cava carries high

pressure venous blood which escapes into the systemic

circulation. Remember the spleen protects against

subsequent infection, especially pneumococcal

pneumonia, malaria and dog & cat bites with

Capnocytophaga canimorsus (a common commensal)

which may rapidly be fatal. Infection is even more

common if HIV is present.

INDICATIONS (OTHER THAN FOR TRAUMA) FOR

SPLENECTOMY

(1) Spontaneous rupture. This is rare, but may occur typically in massive malarial

(not bilharzial) splenomegaly; though it may be truly

spontaneous, e.g. in mononucleosis, the patient may not

remember any trauma because it was slight. It may occur

after colonoscopy. Signs are of shock, left upper

abdominal pain and abdominal distension, although

initially there may be felt a reduction in abdominal girth as

a large spleen bleeds.

(2) Hypersplenism. A big spleen may be responsible for removing all the

blood cell lines, resulting in anaemia, leucopenia and

thrombocytopenia of varying severity, though the

thrombocytopenia is commonest. The problem is that the

same picture can be shown by HIV disease, which itself

can give rise to splenomegaly. Thrombocytopenia is a

serious hazard in surgery and so you need to have some

experience before attempting a splenectomy without

platelets available for transfusion. However, your hand

may be forced if a patient continues to bleed elsewhere

because of the thrombocytopenia, particularly if there is

portal hypertension.

If the underlying cause is HIV disease, blood counts will

improve with ARV therapy (5.8) without splenectomy.

You should anyway be wary of removing a spleen when

there is HIV disease because of the risks of infection;

you may be able to make the distinction between

hypersplenism and HIV-pancytopenia by looking at a bone

marrow film: this is normal or hyperplastic in

hypersplenism, but hypoplastic in HIV disease.

(3) Chronic idiopathic thrombocytopenia. Here the low platelet count is not associated with an

enlarged spleen but through destruction of platelets by

antibodies. There are often ‘megathrombocytes’ in the

peripheral blood film and raised numbers of

megakaryocytes in the bone marrow.

It occurs more often in females than males (4:1);

there is usually quite a good response to prednisolone,

but eventually this option becomes undesirable in the

chronic case.

However splenectomy may not benefit 20% of cases.

Do not do it if systemic lupus erythematosus or rheumatoid

arthritis is the cause of the chronic thrombocytopenia.

Never do it for the acute thrombocytopenia, and especially

not where thrombocytopenia is due to drug sensitivity

(especially quinine). If you have access to radiotherapy

this may be the safer option.

(4) Haemolytic anaemias.

There are several haemoglobinopathies, including sickle

cell trait (never sickle cell disease) thalassaemia, and

spherocytosis for which splenectomy may be beneficial,

but their selection needs the advice of an expert.

(5) Splenic torsion or wandering spleen.

These are both very rare and arise when the spleen has an

abnormally long pedicle and no adhesive attachments.

You are unlikely to make the diagnosis before you operate.

Torsion of the spleen tends to occur during pregnancy

when it is confused with an ovarian tumour!

(6) Hydatid cyst (15.12).

(7) Malignancy. HIV-ve lymphoma, Schistosomiasis related giant follicular

lymphoma, chronic myeloid or lymphatic leukaemia,

or fibrosarcoma affecting only the spleen, but you should

get advice from an expert.

KASHY (20yrs) complained of a swelling in the right iliac fossa.

Ordinarily, it was painless but during attacks of 'fever' it became painful and tender. At laparotomy, the whole spleen was found to be in the right

iliac fossa, but the splenic vessels crossed the abdomen to their normal

position. The 'wandering spleen' was removed easily. LESSON Some rare conditions have easy solutions.

CONTRA-INDICATIONS TO SPLENECTOMY

(1) Splenic abscess (15.18) occurs occasionally. It starts

acutely, it may become chronic, and it shows up

radiologically as a fluid level in an irregular space.

Ultrasound shows the spleen to be filled with dense fluid.

The pus is sterile usually, but may be secondary to

amoebiasis, brucellosis, salmonellosis, leptospirosis or

candidiasis. There may be sickle cell disease, acute

myeloid leukaemia or pancreatitis. Carefully pack away

other abdominal viscera, and drain the abscess: do not try

to remove the spleen.

(2) Tropical splenomegaly syndrome

This is an immune response to recurrent attacks of malaria,

and is responsible for nearly all large spleens in malarious

areas. It responds to long courses of antimalarials.

Do not remove such spleens unless hypersplenism is a

complication.

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(3) Splenic tuberculosis (16.5).

Anti-TB therapy should make splenectomy superfluous;

fibrosis during healing will shrink the spleen. HIV disease

is particularly likely.

(4) Leishmaniasis (34.7). Medication should likewise

make splenectomy unnecessary.

(5) Acute diseases, viz. leptospirosis, acute thrombo-

cytopenia.

(6) HIV disease (5.6).

Whilst not an absolute rule, the risk of infection increases,

and so the indication must be really good. Institute ARV

treatment first.

CAUTION!

(1);Do not operate lightly; your only absolute indications

for doing so are the first three.

(2);If the spleen is huge, think seriously about operating

because it may need a thoraco-abdominal approach.

SPLENECTOMY (GRADE 3.4)

PREPARATION.

Make sure you have a wide bore cannula in place for fluid

replacement; have blood cross-matched (but do not be in a

hurry to raise the haemoglobin if this has been chronically

low), and a nasogastric tube to decompress the stomach.

Provided there is no allergy, always give prophylactic

penicillin perioperatively. Place a sandbag or pillow

behind the left thorax to rotate it to the right.

INCISION. Make a midline or left subcostal incision:

this will give better direct access to the spleen, and you

can extend this as a chevron with a right subcostal

incision. Alternatively for a very big malarial spleen,

you can make a left thoraco-abdominal incision, because

this allows you to see vascular diaphragmatic adhesions

directly. (11.1)

Doing an elective splenectomy is different from an

emergency splenectomy in that you can approach the

spleen in a relaxed manner. Explore the abdomen,

noting the condition of the liver and presence of any

lymph nodes, as well as the mobility of the spleen.

If it is adherent, and large, it is wisest to tie the splenic

vessels first.

You can improve access by placing a pack behind the

spleen if there are insignificant adhesions. Otherwise

divide the peritoneal attachments. If bleeding is a problem

at this stage, deliver the spleen, rotate it forwards to the

right and tie a thick ligature right round the entire splenic

pedicle. This is safer than trying to grasp it with a large

clamp. As you do so, try not to damage the stomach,

and try to cause the least possible damage to the pancreas.

When you have controlled bleeding, proceed to tie the

vessels individually.

Enter the lesser sac by opening a window in the greater

omentum, and lift up the stomach off the pancreas by

dividing the adhesions between them a short distance.

Then feel for the splenic artery along the upper border of

the pancreas. Incise the peritoneum over it, pass an angled

haemostat underneath it and pass ligatures round it.

Carefully expose the splenic vein by dissecting away the

fatty tissue in the pedicle and tie it off. You can then tie off

the splenic artery and divide the splenic pedicle.

For extra security apply a second set of ligatures at the

same point before the vessels divide.

CAUTION! Make sure you pass the ligatures and tie

them before dividing the vessels. If you use haemostats

and the cut vessel drops off and is lost in a pool of blood,

you may never find it again.

If you haven’t been able to draw the spleen forwards,

do so now, if necessary by dividing adhesions to the

parietal peritoneum. Then divide the peritoneum lateral to

the spleen (the lienorenal ligament); put your finger into

the opening and gently free the spleen. You can now bring

it well outside the abdomen. Free the splenic flexure of the

colon from the spleen and separate the tail of the pancreas

from the splenic vessels. Free the spleen from its

attachments to the greater curvature of the stomach by

dividing the short gastric vessels individually in the

gastrosplenic ligament.

CAUTION! Do not include an area of stomach wall

with your ligatures, especially at the upper margin of the

spleen.

Remove the spleen, keeping it in saline for possible

autotransplantation (see below), and put a big dry pack in

the splenic bed. Leave it there for 5mins; then remove it

and look for any bleeding vessels and tie them off.

If the operative site is not absolutely dry and you are

uncertain about an injury to the tail of the pancreas, place a

large drain in the splenic bed.

SPLENIC IMPLANTATION. This is controversial and

may not work. Keep some slices of spleen, say 5x3x0·5cm,

and implant them under the peritoneum in the side wall of

the abdomen, or in the anterior abdominal wall. Or, place

some 1cm cubes of spleen within a sandwich of omentum.

They will usually take, and may reduce the severity of

attacks of malaria and perhaps the danger of septicaemia,

but will not fully protect against pneumococci.

The risk of adhesions is much less than the risk of

life-threatening infections. You can check if the splenic

slices are functional after 4wks if there are no Howell-Jolly

bodies and no target cells in the peripheral blood film,

and the platelet count is normal.

Do not do this with splenectomy indications 4,5,6 or if

there is already an accessory spleen.

SEGMENTAL SPLENECTOMY (GRADE 3.5)

Preserving a functional remnant of c. 20-30% of the spleen

avoids septic and immunological problems also; it can also

be used in hypersplenism. You need to devascularize

anatomical segments (especially middle and lower

portions) of the spleen, by ligating branches of the splenic

artery at the hilum.

Wait for 5mins to observe a line of demarcation, and cut it

along this line in a V-shape whilst squeezing the proximal

portion manually. A vascular clamp across the pedicle will

reduce bleeding. Then sew over the remnant an omental

patch, bringing the edges of the ‘V’ together. This is not

easy surgery.

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DIFFICULTIES WITH SPLENECTOMY

If you have damaged the stomach or the colon, close the

perforation in two layers with long-acting absorbable

suture, make sure nasogastric suction is in place.

Start gentamicin and metronidazole.

If you have damaged the pancreas, suture a piece of

omentum over the damaged segment of pancreas and leave

a drain. Try to monitor the amylase levels of fluid draining

If bleeding from the diaphragm persists, insert one or

two dry packs for 10mins by the clock; then come back

and remove them to see if you can identify the bleeding

vessels to tie them. If you still fail to control bleeding,

leave packs tightly in situ, close the abdomen, and return

after 48hrs to remove them by which time the bleeding

will almost certainly have stopped.

If shock suddenly develops postoperatively, a ligature

has probably come off. Reopen the abdomen immediately,

with good suction available to try to find the bleeding

vessel, and tie it off.

If the wound sloughs and there is a fluid discharge,

the tail of the pancreas or stomach may have been injured.

Reopen the wound, and suture a piece of omentum over

the damaged viscus; do not try to ligate the pancreas or

suture the gastric perforation as sutures will probably cut

out and cause more damage.

If there is fever with no obvious cause, and you have

given penicillin, check for a subphrenic abscess (10.2).

If there is rapidly developing haemolytic anaemia and

fever, suspect malaria or babesiosis, a tick-borne illness

usually affecting domestic or wild animals, and get both

thick and thin blood films. Use quinine 650mg orally tid

and clindamycin 600mg orally tid for 5-10days.

If there is respiratory distress postoperatively, think of

a pneumothorax.

POSTOPERATIVE CARE AFTER SPLENECTOMY

Treat with penicillin prophylactically for 2wks, and longer

in children <2yrs. If you can get it, pneumococcus,

haemophilus and meningococcus vaccine is very

beneficial. Insist on malaria prophylaxis in endemic areas,

including the perioperative period.

15.18 Splenic abscess

This starts acutely, though it may become chronic.

It occurs in sickle cell disease, acute myeloid leukaemia,

HIV+ve patients with candidiasis, and secondary to

amoebiasis, brucellosis, salmonellosis, leptospirosis and

occasionally as a result of acute pancreatitis or perforation

from a gastric ulcer. The danger is rupture into the

peritoneal or pleural cavity and may be accompanied by

disastrous bleeding.

There is left upper abdominal pain, a dragging sensation in

the abdomen, discomfort after meals, anorexia, and a

palpable tender mass extending down from the left upper

quadrant towards the right lower quadrant. This might be

huge. There is usually anaemia and a low-grade fever.

The mass may be tympanic because it usually is filled with

gas, arising from oxygen liberated by red cells in the

spleen, and carbon dioxide from tissue metabolism rather

than gas-forming organisms.

SPECIAL TESTS. Leucocytosis and anaemia are usual,

but the white count may not be raised with HIV disease.

CHEST RADIOGRAPH. An erect film will show a gas

bubble and fluid level below the left hemidiaphragm,

pushing it upwards.

ULTRASOUND. Look for a fluid-filled cavity in the area

of the spleen (38.2F). Much of the splenic tissue may be

destroyed. Aspiration will confirm the diagnosis, but

beware of causing severe haemorrhage or rupturing the

colon. You may be able to aspirate a splenic abscess

completely, and avoid surgery. Treat with antibiotics 48hrs

beforehand and then follow a procedure as for a liver

abscess (15.10).

LAPAROTOMY FOR SPLENIC ABSCESS (GRADE 3.1)

INDICATIONS. Essentially all splenic abscesses need

surgery.

PREPARATION. Cross-match blood and start

pre-operative penicillin and metronidazole.

EXPLORATION. Make a left subcostal incision or

Chevron (inverted-V double subcostal) for very big

abscesses. Pack away the rest of the abdominal contents.

Drain the abscess and leave a large tube or catheter in the

space, passed through a separate stab incision in the lateral

abdominal wall. Lavage the abdomen with warm saline or

water.

DIFFICULTIES WITH SPLENIC ABSCESS

If access is difficult and you have made a midline incision

not expecting a splenic abscess, extend it as an inverted-L

laterally with a left subcostal arm, as a left-sided Kocher

incision (11-1).

If serious bleeding from the spleen ensues, pack the area

and press firmly. Get assistance. Place a further pack

(or two) above and behind the spleen to lift it forward,

and perform a splenectomy (15.17). If you are

experienced, this is the definitive operation rather than

simple drainage.

If you find a gastric perforation, the tissues will be very

friable. Don’t attempt to close the perforation with sutures,

but stuff a segment of omentum into the hole, and fix it

there with absorbable sutures. Make sure you drain the

stomach with a nasogastric tube. You are unlikely to be

able to save the spleen because unravelling the inflamed

tissues will damage it and result in considerable bleeding.

Grasp the hilum of the spleen, place a pack or two behind

it, and perform a splenectomy (15.17)